QC, Quercetin: Click to Expand ⟱
Features:
Plant pigment (flavonoid) found in red wine, onions, green tea, apples and berries.
Quercetin is thought to contribute to anticancer effects through several mechanisms:
-Antioxidant Activity:
-Induction of Apoptosis:modify Bax:Bcl-2 ratio
-Anti-inflammatory Effects:
-Cell Cycle Arrest:
-Inhibition of Angiogenesis and Metastasis: (VEGF)

Cellular Pathways:
-PI3K/Akt/mTOR Pathway: central to cell proliferation, survival, and metabolism.
-MAPK/ERK Pathway: influencing cell proliferation, differentiation, and apoptosis.
-NF-κB Pathway: downregulate NF-κB
-JAK/STAT Pathway: interfere with the activation of STAT3
-Apoptotic Pathways: intrinsic (mitochondrial) and extrinsic (death receptor-mediated) pathways

Quercetin has been used at doses around 500–1000 mg per day
Quercetin’s bioavailability from foods or standard supplements can be low.

-Note half-life 11 to 28 hours.
BioAv low 1-10%, poor water-solubility, consuming with fat may improve bioavialability. also piperine or VitC.
Pathways:
- induce ROS production in cancer cells (higher dose). Typicallys Lowers ROS in normal cells(unless it is high dose?)or depends on Redox status?. "quercetin paradox"
- ROS↑ related: MMP↓(ΔΨm), ER Stress↑, UPR↑, GRP78↑, Ca+2↑, Cyt‑c↑, Caspases↑, DNA damage↑, cl-PARP↑, HSP↓, Prx,
- Confusing info about Lowering AntiOxidant defense in Cancer Cells: NRF2↓(some contrary), Trx&wNotes=on">TrxR↓**, SOD↓(contrary), GSH↓ Catalase↓(contrary), HO1↓(some contrary), GPx↓(some contrary)
- Raises AntiOxidant defense in Normal Cells: ROS↓, NRF2↑, SOD↑, GSH↑, Catalase↑,
- lowers Inflammation : NF-kB↓, COX2↓, p38↓, Pro-Inflammatory Cytokines : NLRP3↓, IL-1β↓, TNF-α↓, IL-6↓, IL-8↓
- inhibit Growth/Metastases : TumMeta↓, TumCG↓, EMT↓, MMPs↓, MMP2↓, MMP9↓, TIMP2, IGF-1↓, uPA↓, VEGF↓, ROCK1↓, FAK↓, NF-κB↓, CXCR4↓, SDF1↓, TGF-β↓, α-SMA↓, ERK↓
- reactivate genes thereby inhibiting cancer cell growth : HDAC↓, DNMTs↓, EZH2↓, P53↑, HSP↓, Sp proteins↓, TET↑
- cause Cell cycle arrest : TumCCA↑, cyclin D1↓, cyclin E↓, CDK2↓, CDK4↓, CDK6↓,
- inhibits Migration/Invasion : TumCMig↓, TumCI↓, TNF-α↓, FAK↓, ERK↓, EMT↓, TOP1↓, TET1,
- inhibits glycolysis and ATP depletion : HIF-1α↓, PKM2↓, cMyc↓, GLUT1↓, LDH↓, LDHA↓, HK2↓, PFKs↓, PDKs↓, ECAR↓, OXPHOS↓, GRP78↑, GlucoseCon↓
- inhibits angiogenesis↓ : VEGF↓, HIF-1α↓, Notch↓, FGF↓, PDGF↓, EGFR↓,
- some indication of inhibiting Cancer Stem Cells : CSC↓, CK2↓, Hh↓, CD24↓, β-catenin↓, Notch2↓,
- Others: PI3K↓, AKT↓, JAK↓, STAT↓, Wnt↓, β-catenin↓, AMPK, α↓, ERK↓, JNK, - SREBP (related to cholesterol).
- Synergies: chemo-sensitization, chemoProtective, RadioSensitizer, RadioProtective, Others(review target notes), Neuroprotective, Cognitive, Renoprotection, Hepatoprotective, CardioProtective,

- Selectivity: Cancer Cells vs Normal Cells


Scientific Papers found: Click to Expand⟱
25- EGCG,  QC,    Quercetin Increased the Antiproliferative Activity of Green Tea Polyphenol (-)-Epigallocatechin Gallate in Prostate Cancer Cells
- in-vitro, Pca, PC3 - in-vitro, Pca, LNCaP
COMT↓,

26- EGCG,  QC,  docx,    Green tea and quercetin sensitize PC-3 xenograft prostate tumors to docetaxel chemotherapy
- vitro+vivo, Pca, PC3
BAD↓,
PARP↑,
Casp7↑,
IκB↓,
Ki-67↓,
VEGF↓,
EGFR↓,
FGF↓,
TGF-β↓,
TNF-α↓,
SCF↓,
Bax:Bcl2↑,
NF-kB↓,

24- EGCG,  GEN,  QC,    Targeting CWR22Rv1 prostate cancer cell proliferation and gene expression by combinations of the phytochemicals EGCG, genistein and quercetin
- in-vitro, Pca, 22Rv1
NQO1↑,
P53↑,
NQO2↑,

2458- EGCG,  QC,    Identification of plant-based hexokinase 2 inhibitors: combined molecular docking and dynamics simulation studies
- Analysis, Nor, NA
HK2↓, Overall, this study concludes that EGCG and quercitrin might possess the inhibitory potential for HK2.

2642- Flav,  QC,  Api,  KaempF,  MCT  In Vitro–In Vivo Study of the Impact of Excipient Emulsions on the Bioavailability and Antioxidant Activity of Flavonoids: Influence of the Carrier Oil Type
- in-vitro, Nor, NA - in-vivo, Nor, NA
*BioAv↑, Overall, the bioavailability and antioxidant activity of flavonoids increased when they were coingested with excipient emulsions.
*eff↝, However, in vivo pharmacokinetic experiments showed that the flavonoid concentrations in rat serum were comparable for all carrier oils
BioEnh↑, MCT is the bioenhancer for the Flavonoids (which have low soluability in water)

1997- Myr,  QC,    Inhibition of Mammalian thioredoxin reductase by some flavonoids: implications for myricetin and quercetin anticancer activity
- in-vitro, Lung, A549
TrxR↓, Myricetin and quercetin were found to have strong inhibitory effects on mammalian TrxRs with IC50 values of 0.62 and 0.97 micromol/L, respectively
eff↑, Oxygen-derived superoxide anions enhanced the inhibitory effect whereas anaerobic conditions attenuated inhibition.
TumCCA↑, cell cycle was arrested in S phase by quercetin and an accumulation of cells in sub-G1 was observed in response to myricetin.
eff↓, presence of superoxide dismutase diminished the inhibition dramatically
ROS↑, show that ROS played a critical role in the inhibition of TrxR by flavonoids. ...may occur as a result of their easy oxidization to flavonol semiquinone species.

981- NarG,  QC,    Anti-estrogenic and anti-aromatase activities of citrus peels major compounds in breast cancer
- in-vivo, NA, NA
TumVol↓,
CYP19↓, Reduction in aromatase levels in solid tumors was also observed in treated groups (Aromatase inhibitor)

980- QC,    Dietary Quercetin Exacerbates the Development of Estrogen-Induced Breast Tumors in Female ACI Rats
- in-vivo, BC, NA
COMT↓, bad
ROS∅, quercetin (2.5 g/kg food) does not confer protection against breast cancer, does not inhibit E2-induced oxidant stress and may exacerbate breast carcinogenesis in E2-treated ACI rats.

3337- QC,    Endoplasmic Reticulum Stress-Relieving Effect of Quercetin in Thapsigargin-Treated Hepatocytes
- in-vitro, NA, HepG2
*Inflam↓, quercetin exerts anti-inflammatory and anti–insulin resistance actions by suppressing UPR in cells experiencing ER stress
*UPR↓,
*GRP58↓, (GRP78) and the downstream proteins such as X-box binding protein 1 (XBP1). The increased expression was significantly inhibited by quercetin, indicating that this compound can relieve ER stress
*XBP-1↓,
*ER Stress↓, previous reports as well as our results, we suggest that quercetin can inhibit ER stress in hepatocytes
*antiOx↑, Quercetin, a well-known antioxidant, is one of the most abundant flavonols in vegetables and fruits and has been shown to have many pharmacological actions
TNF-α↓, Quercetin suppressed the increased expression of TNF-α significantly and dose-dependently
p‑eIF2α↓, quercetin treatment suppressed the phosphorylation of eIF2α, IRE1α and JNK and the mRNA expression of XBP-1, GRP78 and CHOP
p‑IRE1↓,
p‑JNK↓,
CHOP↓,

1201- QC,    Quercetin: a silent retarder of fatty acid oxidation in breast cancer metastasis through steering of mitochondrial CPT1
- in-vivo, BC, NA
mitResp↓, significant reduction in the intracellular mitochondrial respiration
Glycolysis↓,
ATP↓,
ROS↑,
GSH↓,
TumMeta↓,
Apoptosis↑,
FAO↓,

1493- QC,    New quercetin-coated titanate nanotubes and their radiosensitization effect on human bladder cancer
- NA, Bladder, NA
RadioS↑,
ChemoSen↑,

2300- QC,    Flavonoids Targeting HIF-1: Implications on Cancer Metabolism
- Review, Var, NA
AntiTum↑, Quercetin exerts promising anti-tumor effects via the regulation of various cancer signaling pathways
Hif1a↓, Quercetin inhibited HIF-1 transcriptional activity in the HCT116 colon cancer cell line
*Hif1a↑, On the contrary, quercetin increased the accumulation of HIF-1α in healthy cells
Glycolysis↓, Quercetin inhibited glycolysis and proliferation of glycolysis-dependent hepatocellular carcinoma (SMMC-7721 and Bel-7402) cells by downregulating HKII;
HK2↓,
PDK3↓, quercetin inhibited PDK3 in hepatocellular carcinoma (HepG2) and lung cancer (A549) cells
PFKP?, The ability of quercetin to impair PFKP-LDHA signaling

2303- QC,  doxoR,    Quercetin greatly improved therapeutic index of doxorubicin against 4T1 breast cancer by its opposing effects on HIF-1α in tumor and normal cells
- in-vitro, BC, 4T1 - in-vivo, NA, NA
cardioP↑, Quercetin had better cardioprotective and hepatoprotective activities.
hepatoP↑,
TumCG↓, In vivo, quercetin suppressed tumor growth and prolonged survival in BALB/c mice bearing 4T1 breast cancer.
OS↑,
ChemoSen↑, quercetin enhanced therapeutic efficacy of DOX and simultaneously reduced DOX-induced toxic side effects
chemoP↑, IC50 of DOX in combination with quercetin 10 or 25 uM was increased by three- and fourfold, respectively, compared with that of DOX alone
Hif1a↓, Further study showed that quercetin suppressed intratumoral HIF-1α in a hypoxia-dependent way but increased its accumulation in normal cells
*Hif1a↑,
selectivity↑, quercetin could improve therapeutic index of DOX by its opposing effects on HIF-1α in tumor and normal cells
TumVol↓,
OS↑,

2338- QC,    Quercetin: A Flavonoid with Potential for Treating Acute Lung Injury
- Review, Nor, NA
*SIRT1↑, Quercetin increased SIRT1 expression in lung tissue, inhibited NLRP3 inflammasome activation, and reduced the release of pro-inflammatory factors (TNFα, IL-1β, and IL-6), preventing the up-regulation of nuclear PKM2 in the lung.
*NLRP3↓,
*Inflam↓,
*TNF-α↓,
*IL1β↓,
*IL6↓,
*PKM2↓, preventing the up-regulation of nuclear PKM2 in the lung.
*HO-1↑, Quercetin increased HO-1 expression in the lungs of a septic lung injury mouse model
*ROS↓, puncture in rats, showing that early administration of Quercetin reduced the levels of oxidative stress markers, such as xanthine oxidase (XO), nitric oxide (NO), and malondialdehyde (MDA), and increased the levels of antioxidant enzymes in lung tiss
*NO↓,
*MDA↓,
*antiOx↑,
*COX2↓, Quercetin also reduced the expression of COX-2, HMGB1, and iNOS expression and NF-κB p65 phosphorylation
*HMGB1↓,
*iNOS↓,
*NF-kB↓,

2339- QC,    Quercetin protects against LPS-induced lung injury in mice via SIRT1-mediated suppression of PKM2 nuclear accumulation
- in-vivo, Nor, NA
*Inflam↓, Quercetin (Que) is a natural bioflavonoid compound with anti-inflammatory and antioxidative properties that reportedly inhibits the NLRP3 inflammasome in sepsis-induced organ dysfunctions such as ALI
*antiOx↑,
*NLRP3↓,
*Sepsis↓,
*PKM2↓, inhibit the activation of the NLRP3 inflammasome by suppressing the nuclear accumulation of PKM2 and increasing SIRT1 levels.
*SIRT1↓,

2340- QC,    Oral Squamous Cell Carcinoma Cells with Acquired Resistance to Erlotinib Are Sensitive to Anti-Cancer Effect of Quercetin via Pyruvate Kinase M2 (PKM2)
- in-vitro, OS, NA
TumCG↓, At a concentration of 5 μM, quercetin effectively arrested cell growth, reduced glucose utilization, and inhibited cellular invasiveness
GlucoseCon↓,
TumCI↓,
GLUT1↓, Quercetin also prominently down-regulated GLUT1, PKM2, and lactate dehydrogenase A (LDHA) expression of erlotinib-resistant HSC-3 cells
PKM2↓,
LDHA↓,
Glycolysis↓, Moreover, quercetin (30 μM) suppressed glycolysis in the MCF-7 and MDA-MB-231 breast cancer cells, as evidenced by decreased glucose uptake and lactate production with a concomitant decrease in the levels of the GLUT1, PKM2, and LDHA proteins [29].
lactateProd↓,
HK2↓, Hexokinase 2 (HK2)-mediated glycolysis was also shown to be inhibited following quercetin treatment (25~50 μM) in Bel-7402 and SMMC-7721 hepatocellular carcinoma (HCC) cells
eff↑, Downregulation of PKM2 also potently restored sensitivity to the inhibitory effect of erlotinib on cell growth and invasion

2341- QC,    Quercetin suppresses the mobility of breast cancer by suppressing glycolysis through Akt-mTOR pathway mediated autophagy induction
- in-vitro, BC, MCF-7 - in-vitro, BC, MDA-MB-231 - in-vivo, NA, NA
MMP2↓, quercetin treatment down-regulated the expression of cell migration marker proteins, such as matrix metalloproteinase 2 (MMP-2), MMP-9 and vascular endothelial growth factor (VEGF).
MMP9↓, level of MMP-2, MMP-9 and VEGF was all strongly cut down by quercetin treatment compared with control group
VEGF↓,
Glycolysis↓, quercetin successfully blocked cell glycolysis by inhibiting the level of glucose uptake and the production of lactic acid
lactateProd↓,
PKM2↓, and also decreased the level of glycolysis-related proteins Pyruvate kinase M2 (PKM2), Glucose transporter1(GLUT1) and Lactate dehydrogenase A (LDHA).
GLUT1↓,
LDHA↓,
TumAuto↑, quercetin induced obvious autophagy via inactivating the Akt-mTOR pathway
Akt↓,
mTOR↓,
TumMeta↓, Quercetin suppressed the progression of breast cancer by inhibiting tumor metastasis and glycolysis in vivo
MMP3↓, quercetin effectively suppressed the invasion and migration ability of breast cancer cells through suppressing the expression of MMP-3, MMP-9 and VEGF,
eff↓, down-regulating the expression of PKM2, which regulated the final step of glycolysis, could effectively enhance the chemotherapeutic effect of THP
GlucoseCon↓, we found that quercetin effectively suppressed the level of glucose uptake and the production of lactic acid, and also down-regulated the expression of glycolysis-related proteins PKM2, LDHA and GLUT1,
lactateProd↓,
TumAuto↑, quercetin treatment induced obvious autophagy in MCF-7 and MDA-MB-231 cells via inactivating the Akt-mTOR pathway
LC3B-II↑, showing obvious conversion of LC3B-I to LC3B-II

2342- QC,    Quercetin Inhibits the Proliferation of Glycolysis-Addicted HCC Cells by Reducing Hexokinase 2 and Akt-mTOR Pathway
- in-vitro, HCC, Bel-7402 - in-vitro, HCC, SMMC-7721 cell - in-vivo, NA, NA
TumCP↓, In the present study, we reported that QUE inhibited the proliferation of HCC cells that relied on aerobic glycolysis.
HK2↓, QUE could decrease the protein levels of HK2 and suppress the AKT/mTOR pathway in HCC cells
Akt↓,
mTOR↓,
GlucoseCon↓, glucose uptake and lactate production of SMMC-7721 and Bel-7402 decreased in a dose-dependent manner after QUE treatment
lactateProd↓,
Glycolysis↓, QUE can inhibit the glycolysis of cancer cells, thereby inhibiting the progression of multiple cancers

2343- QC,    Pharmacological Activity of Quercetin: An Updated Review
- Review, Nor, NA
*ROS↓, Quercetin is a potent scavenger for ROS and hence protects the body against oxidative stress
*GSH↓, Studies of animals and cells have shown that the synthesis of GSH is induced by quercetin.
*Catalase↑, increased expression of superoxide dismutase (SOD), catalase (CAT), and GSH has been reported with the pretreatment of quercetin
*SOD↑,
*MDA↓, quercetin supplementation to layer chickens significantly reduced malondialdehyde (MDA) levels in the kidneys, liver, and heart and increased GSH, CAT, and glutathione peroxidase (GSH-Px) activities in the liver, kidney, and heart tissue
*GPx↑,
*Copper↓, In addition, quercetin can exert antioxidant effects by chelating Cu2+ and Fe2+ in its structure with catechol
*Iron↓,
Apoptosis↓, Quercetin inhibits the proliferation of liver cancer cells via induction of apoptosis and cell cycle arrest [43].
TumCCA↑,
MMP2↓, In HSC-6, SCC-9 human oral cancer cell lines, quercetin inhibits cell viability, migration, and invasion, reduces MMP-2 and MMP-9 abundance, downgrades miR-16, and upgrades HOXA10
MMP9↓,
GlucoseCon↓, quercetin inhibits the mobility of cancer cells by inhibiting glucose uptake and lactic acid production and reducing levels of PKM2, GLUT1, and LDHA, which may have a significant role in controlling breast cancer [56].
lactateProd↓,
PKM2↓,
GLUT1↓,
LDHA↓,
ROS↑, Quercetin encapsulated in solid lipid nanoparticles ,MCF-7 and MCF-10A cells, Increase (ROS)

2344- QC,    Quercetin: A natural solution with the potential to combat liver fibrosis
- Review, Nor, NA
*HK2↓, By reducing the activity of key glycolytic enzymes—including hexokinase II (HK2), phosphofructokinase platelet (PFKP), and pyruvate kinase M2 (PKM2)—quercetin lowers energy production in LSECs, potentially slowing fibrosis progression.
*PFKP↓,
*PKM2↓,
*hepatoP↑, Quercetin lowered levels of liver enzymes (ALT, AST) and total bile acid, markers of liver injury.
*ALAT↓,
*AST↓,
*Glycolysis↓, quercetin inhibited glycolysis in LSECs, reducing lactate production, glucose consumption, and the expression of glycolytic enzymes
*lactateProd↓,
*GlucoseCon↓,
*CXCL1↓, By suppressing CXCL1 secretion, quercetin decreased neutrophil infiltration, a key factor in liver fibrosis, thereby effecting inflammation control.
*Inflam↓,

2431- QC,    The Protective Effect of Quercetin against the Cytotoxicity Induced by Fumonisin B1 in Sertoli Cells
- in-vitro, Nor, TM4
*Apoptosis↓, 40 μM quercetin improved cell viability, reduced apoptosis, and preserved cell functions.
*ROS↓, Quercetin also decreased reactive oxygen species (ROS) levels in TM4 cells exposed to FB1
*antiOx↓, enhanced the expression of antioxidant genes
*MMP↑, improved mitochondrial membrane potential.
*GPI↑, elevated the mRNA and protein expression of glycolysis-related genes, including (Gpi1), (Hk2), (Aldoa), (Pkm), lactate (Ldha) and (Pfkl)
*HK2↑,
*ALDOA↑,
*PKM1↑,
*LDHA↑,
*PFKL↑,

3334- QC,    Pharmacokinetics of Quercetin Absorption from Apples and Onions in Healthy Humans
- Trial, Nor, NA
*Half-Life↑, elimination half-time (t1/2 ) of females (93.8 h for AP and 15.2 h for OP) was much higher than that of males t1/2 of (29.9 h for AP and 13.4 h for OP).

3335- QC,    Recent advances on the improvement of quercetin bioavailability
- Review, NA, NA
*BioAv↓, bioavailability of quercetin is relatively low (<10%)

3336- QC,    Neuroprotective Effects of Quercetin in Alzheimer’s Disease
- Review, AD, NA
*neuroP↑, Neuroprotection by quercetin has been reported in several in vitro studies
*lipid-P↓, It has been shown to protect neurons from oxidative damage while reducing lipid peroxidation.
*antiOx↑, In addition to its antioxidant properties, it inhibits the fibril formation of amyloid-β proteins, counteracting cell lyses and inflammatory cascade pathways.
*Aβ↓,
*Inflam↓,
*BBB↓, It also has low BBB penetrability, thus limiting its efficacy in combating neurodegenerative disorders.
*NF-kB↓, downregulating pro-inflammatory cytokines, such as NF-kB and iNOS, while stimulating neuronal regeneration
*iNOS↓,
*memory↑, Quercetin has shown therapeutic efficacy, improving learning, memory, and cognitive functions in AD
*cognitive↑,
*AChE↓, Quercetin administration resulted in the inhibition of AChE
*MMP↑, quercetin ameliorates mitochondrial dysfunction by restoring mitochondrial membrane potential, decreases ROS production, and restores ATP synthesis
*ROS↓,
*ATP↑,
*AMPK↑, It also increased the expression of AMP-activated protein kinase (AMPK), which is a key cell regulator of energy metabolism.
*NADPH↓, Activated AMPK can decrease ROS generation by inhibiting NADPH oxidase activity
*p‑tau↓, Inhibition of AβAggregation and Tau Phosphorylation

903- QC,    Potential toxicity of quercetin: The repression of mitochondrial copy number via decreased POLG expression and excessive TFAM expression in irradiated murine bone marrow
- in-vivo, NA, NA
ROS⇅, antioxidant and prooxidant effects largely relates to its dose

913- QC,    Effects of low dose quercetin: Cancer cell-specific inhibition of cell cycle progression
- in-vitro, BC, SkBr3 - in-vitro, BC, MDA-MB-435
TumCP↓,
TumCCA↑, arrest at the G1 phase
DNAdam↑, mild DNA damage
Chk2↑,
CycB↓, cyclin B1
CDK1↓,
tumCV↓, 94% viability with 10uM
p‑RB1↓, Rb
P21↑,

3534- QC,  Lyco,    Synergistic protection of quercetin and lycopene against oxidative stress via SIRT1-Nox4-ROS axis in HUVEC cells
- in-vitro, Nor, HUVECs
*ROS↓, especially quercetin-lycopene combination (molar ratio 5:1), prevented the oxidative stress in HUVEC cells by reducing the reactive oxygen species (ROS) and suppressing the expression of NADPH oxidase 4 (Nox4), a major source of ROS production.
*NOX4↓, Quercetin-lycopene combination could interact with SIRT1 to inhibit Nox4 and prevent endothelial oxidative stress
*Inflam↓, quercetin-lycopene combination downregulated inflammatory genes induced by H2O2, such as IL-17 and NF-κB.
*NF-kB↓, NF-κB p65 was activated by H2O2 but inhibited by the quercetin-lycopene combination.
*p65↓,
*SIRT1↑, quercetin and lycopene combination promoted the thermostability of Sirtuin 1 (SIRT1) and activated SIRT1 deacetyl activity
*cardioP↑, The cardioprotective role of SIRT1
*IL6↓, LYP: Q = 1:5), interacted with deacetylase SIRT1 to inhibit NF-κB p65 and Nox4 enzyme, downregulated inflammatory cytokines such as IL-6 and pro-inflammatory enzymes such as COX-2, and suppressed ROS elevation activated by H2O2.
*COX2↓,

904- QC,    Antioxidant and prooxidant effects of quercetin on glyceraldehyde-3-phosphate dehydrogenase
- Analysis, NA, NA
ROS↑, Quercetin significantly increased oxidation of GAPDH observed in the presence of ferrous ions
H2O2↑,

905- QC,    Anti- and pro-oxidant effects of quercetin in copper-induced low density lipoprotein oxidation. Quercetin as an effective antioxidant against pro-oxidant effects of urate
- Analysis, NA, NA
ROS↑, pro-oxidant behavior depends on the Cu(2+) concentration

906- QC,    The interplay between reactive oxygen species and antioxidants in cancer progression and therapy: a narrative review
- Review, NA, NA
ROS↑, quercetin at higher concentrations (>50 µM) can initiate ROS generation especially O2•−

907- QC,    A Comprehensive Study on the Anti-cancer Effects of Quercetin and Its Epigenetic Modifications in Arresting Progression of Colon Cancer Cell Proliferation
- Review, NA, NA
AntiCan↑, fascinated attention to quercetin as an anti-inflammatory plant product since it exerts specific effects only on cancer cells rather than on normal

908- QC,    Molecular Targets Underlying the Anticancer Effects of Quercetin: An Update
- Review, NA, NA
AntiCan↑, quercetin exerts anticancer effect by binding to cellular receptors and proteins
ROS↑, The short-term effect causes scavenging of free radicals and it is mostly antioxidative and antiapoptotic in nature, while the long term effect is pro-oxidative

909- QC,    Exploring the therapeutic potential of quercetin in cancer treatment: Targeting long non-coding RNAs
- Review, NA, NA
other↓, quercetin suppresses oncogenic lncRNAs
other↑, while enhancing tumor-suppressive lncRNAs

910- QC,    The Anti-Cancer Effect of Quercetin: Molecular Implications in Cancer Metabolism
tumCV↓,
Apoptosis↑,
PI3k/Akt/mTOR↓, QUE induces cell death by inhibiting PI3K/Akt/mTOR and STAT3 pathways in PEL cells
Wnt/(β-catenin)↓, reducing β-catenin
MAPK↝,
ERK↝, ERK1/2
TumCCA↑, cell cycle arrest at the G1 phase
H2O2↑,
ROS↑,
TumAuto↑,
MMPs↓, Consistently, QUE was able to reduce the protein levels of MMP-2, MMP-9, VEGF and mTOR, and p-Akt in breast cancer cell lines
P53↑,
Casp3↑,
Hif1a↓, by inactivating the Akt-mTOR pathway [64,74] and HIF-1α
cFLIP↓,
IL6↓, QUE decreased the release of interleukin-6 (IL-6) and IL-10
IL10↓,
lactateProd↓,
Glycolysis↓, It is suggested that QUE alters glucose metabolism by inhibiting monocarboxylate transporter (MCT) activity
PKM2↓,
GLUT1↓,
COX2↓,
VEGF↓,
OCR↓,
ECAR↓,
STAT3↓,
MMP2↓, Consistently, QUE was able to reduce the protein levels of MMP-2, MMP-9, VEGF and mTOR, and p-Akt in breast cancer cell lines
MMP9:TIMP1↓,
mTOR↓,

911- QC,  SFN,    Pilot study evaluating broccoli sprouts in advanced pancreatic cancer (POUDER trial) - study protocol for a randomized controlled trial
TumCG↓,
Risk↓, decreased risk of extra-prostatic manifestation of prostate cancer: cruciferous vegetables, in particular broccoli which is rich in sulforaphane and quercetin

912- QC,  2DG,    Selected polyphenols potentiate the apoptotic efficacy of glycolytic inhibitors in human acute myeloid leukemia cell lines. Regulation by protein kinase activities
Apoptosis↑,
ROS↓, 2-DG (5 mM) and Quer (10–40 μM) reduced the basal intracellular ROS content in HL60 cells
GSH∅, GSH levels were not significantly affected by treatment for 3 h
other↑, activated apoptosis throughout the mitochondrial (“intrinsic”) executioner pathway

926- QC,  PacT,  doxoR,  Tam,    Bioenhancers from mother nature and their applicability in modern medicine
- Review, Nor, NA
*BioEnh↑, Piperine, obtained from the oleoresin in the peppercorns is by far the most studied and researched bioenhancer.
BioEnh↑, In a study, pretreatment of quercetin (5.0 and 15 mg/kg) half an hour before verapamil (10 mg/kg) administration significantly altered the pharmacokinetics of verapamil.
BioEnh↑, genistein (10 mg/kg) caused an increase in AUC (54.7%) and a decrease in the total plasma clearance (35.2%) after oral administration of paclitaxel
BioEnh↑, Oral naringin (3.3 and 10 mg/kg) was pretreated 30 min before and after intravenous administration of paclitaxel (3 mg/kg), the AUC was significantly improved (40.8% and 49.1% for naringin doses
BioEnh↑, One of the widely used bioenhancers is Capmul MCM C10, a glyceryl monocaprate, produced from edible fats and oils and is commonly used in lip products.
BioEnh↑, Nitrite glycoside is a bioenhancer for drugs and nutrients. Novel bioactive nitrile glycosides, niaziridin and niazirin is obtained from the leaves, pods, and bark of Moringa oleifera
BioEnh↑, Cow urine distillate is more effective as bioenhancer than cow urine, to increase the effectiveness of antimicrobial, antifungal, and anticancer drugs.
P-gp↓, Bioavailability-enhancing activity of natural compounds from the medicinal plants may be attributed to various mechanisms, such as P-gp inhibition activity by flavone, quercetin, and genistein

914- QC,    Quercetin and Cancer Chemoprevention
- Review, NA, NA
GSH↓, high Qu concentration, causes a reduction in GSH content
ROS↑, in tumor cells
TumCCA↑, Depending on the cell type and tumor origin, Qu is able to block the cell cycle at G2/M or at the G1/S transition
Ca+2↑, Qu treatment increases cytosolic Ca2+ levels
MMP↓,
Casp3↑,
Casp8↑,
Casp9↑,
β-catenin/ZEB1↓,
AMPKα↑,
ASK1↑,
p38↑,
TRAIL↑, Qu is a potent enhancer of TNF-related apoptosis-inducing ligand (TRAIL)-induced apoptosis, through the induction of the expression of death receptor (DR)-5, a phenomenon that specifically occurs in prostate cancer cells
DR5↑,
cFLIP↓,
Apoptosis↑, tumor cell lines are prone to cell-cycle arrest and apoptosis at Qu concentrations that have no or little effect on non-transformed cells ****

915- QC,    Hormesis and synergy: pathways and mechanisms of quercetin in cancer prevention and management
- Review, NA, NA
ROS↑, Pro-oxidant effects are present at cellular concentrations of 40–100uM

916- QC,    Quercetin and cancer: new insights into its therapeutic effects on ovarian cancer cells
- Review, Ovarian, NA
COX2↓,
CRP↓,
ER Stress↑, Quercetin can result in stimulate the ER stress pathway that lead to the cause of cell death and apoptosis
Apoptosis↑,
GRP78/BiP↑,
CHOP↑,
p‑STAT3↓, quercetin suppresses STAT3 and PI3K/AKT/mTOR pathways
PI3K↓,
Akt↓,
mTOR↓,
cMyc↓, leading to downregulate the prosurvival cellular proteins expression, including cMyc, cyclin D1, and c-FLIP
cycD1↓,
cFLIP↓,
IL6↓, decreased the IL-6 and IL-10 release
IL10↓,

917- QC,  BML,  Pap,    Quercetin: A Versatile Flavonoid
- Review, Nor, NA
*BioEnh↑, quercetin was combined with bromelain and papain, which may enhance its absorption and papain, which may enhance its absorption

918- QC,  CUR,  VitC,    Anti- and pro-oxidant effects of oxidized quercetin, curcumin or curcumin-related compounds with thiols or ascorbate as measured by the induction period method
- Analysis, NA, NA
ROS↑, CUR enhances the prooxidant activity of ascorbate(vit C)
ROS↑, Under anaerobic conditions, QUE, with a catechol ring, may be more prooxidant than CUR, with a phenol ring.

919- QC,    Quercetin Regulates Sestrin 2-AMPK-mTOR Signaling Pathway and Induces Apoptosis via Increased Intracellular ROS in HCT116 Colon Cancer Cells
- in-vitro, CRC, HCT116
Apoptosis↑,
ROS↑,
SESN2↑,
P53↑,
AMPKα↑,
mTOR↓,

920- QC,    Interfering with ROS Metabolism in Cancer Cells: The Potential Role of Quercetin
- Review, NA, NA
GSH↓, Qu depletes GSH in a concentration-dependent manner;
ROS↑, Because normal, non-transformed cells have a lower basal intracellular ROS level, and have a full antioxidant capacity, they should be less vulnerable to the ROS stress that is induced by Qu. ****

921- QC,    Essential requirement of reduced glutathione (GSH) for the anti-oxidant effect of the flavonoid quercetin
- in-vitro, lymphoma, U937
ROS↑, long periods it showed a pro-oxidant activity
GSH↓, long periods

922- QC,    Quercetin and ovarian cancer: An evaluation based on a systematic review
- Review, NA, NA
ROS↑, presence of peroxidases, Q reacts with H2O2 to form a Q-quinone (QQ) that has a pro-oxidant effect

923- QC,    Quercetin as an innovative therapeutic tool for cancer chemoprevention: Molecular mechanisms and implications in human health
- Review, Var, NA
ROS↑, decided by the availability of intracellular reduced glutathione (GSH),
GSH↓, extended exposure with high concentration of quercetin causes a substantial decline in GSH levels
Ca+2↝,
MMP↓,
Casp3↑, activation of caspase-3, -8, and -9
Casp8↑,
Casp9↑,
other↓, when p53 is inhibited, cancer cells become vulnerable to quercetin-induced apoptosis
*ROS↓, Quercetin (QC), a plant-derived bioflavonoid, is known for its ROS scavenging properties and was recently discovered to have various antitumor properties in a variety of solid tumors.
*NRF2↑, Moreover, the therapeutic efficacy of QC has also been defined in rat models through the activation of Nrf-2/HO-1 against high glucose-induced damage
HO-1↑,
TumCCA↑, QC increases cell cycle arrest via regulating p21WAF1, cyclin B, and p27KIP1
Inflam↓, QC-mediated anti-inflammatory and anti-apoptotic properties play a key role in cancer prevention by modulating the TLR-2 (toll-like receptor-2) and JAK-2/STAT-3 pathways and significantly inhibit STAT-3 tyrosine phosphorylation within inflammatory ce
STAT3↓,
DR5↑, several studies showed that QC upregulated the death receptor (DR)
P450↓, it hinders the activity of cytochrome P450 (CYP) enzymes in hepatocytes
MMPs↓, QC has also been shown to suppress metastatic protein expression such as MMPs (matrix metalloproteases)
IFN-γ↓, QC is its ability to inhibit inflammatory mediators including IFN-γ, IL-6, COX-2, IL-8, iNOS, TNF-α,
IL6↓,
COX2↓,
IL8↓,
iNOS↓,
TNF-α↓,
cl‑PARP↑, Induced caspase-8, caspase-9, and caspase-3 activation, PARP cleavage, mitochondrial membrane depolarization,
Apoptosis↑, increased apoptosis and p53 expression
P53↑,
Sp1/3/4↓, HT-29 colon cancer cells: decreased the expression of Sp1, Sp3, Sp4 mrna, and survivin,
survivin↓,
TRAILR↑, H460 Increased the expression of TRAILR, caspase-10, DFF45, TNFR 1, FAS, and decreased the expression of NF-κb, ikkα
Casp10↑,
DFF45↑,
TNFR 1↑,
Fas↑,
NF-kB↓,
IKKα↓,
cycD1↓, SKOV3 Reduction in cyclin D1 level
Bcl-2↓, MCF-7, HCC1937, SK-Br3, 4T1, MDA-MB-231 Decreased Bcl-2 expression, increasedBax expression, inhibition of PI3K-Akt pathway
BAX↑,
PI3K↓,
Akt↓,
E-cadherin↓, MDA-MB-231 Induced the expression of E-cadherin and downregulated vimentin levels, modulation of β-catenin target genes such as cyclin D1 and c-Myc
Vim↓,
β-catenin/ZEB1↓,
cMyc↓,
EMT↓, MCF-7 Suppressed the epithelial–mesenchymal transition process, upregulated E-cadherin expression, downregulated vimentin and MMP-2 expression, decreased Notch1 expression
MMP2↓,
NOTCH1↓,
MMP7↓, PANC-1, PATU-8988 Decreased the secretion of MMP and MMP7, blocked the STAT3 signaling pathway
angioG↓, PC-3, HUVECs Reduced angiogenesis, increased TSP-1 protein and mrna expression
TSP-1↑,
CSCs↓, PC-3 and LNCaP cells Activated capase-3/7 and inhibit the expression of Bcl-2, surviving and XIAP in CSCs.
XIAP↓,
Snail↓, inhibiting the expression of vimentin, slug, snail and nuclear β-catenin, and the activity of LEF-1/TCF responsive reporter
Slug↓,
LEF1↓,
P-gp↓, MCF-7 and MCF-7/dox cell lines Downregulation of P-gp expression
EGFR↓, MCF-7 and MDA-MB-231 cells Suppressed EGFR signaling and inhibited PI3K/Akt/mTOR/GSK-3β
GSK‐3β↓,
mTOR↓,
RAGE↓, IA Paca-2, BxPC3, AsPC-1, HPAC and PANC1 Silencing RAGE expression
HSP27↓, Breast cancer In vivo NOD/SCID mice Inhibited the overexpression of Hsp27
VEGF↓, QC significantly reversed an elevation in profibrotic markers (VEGF, IL-6, TGF, COL-1, and COL-3)
TGF-β↓,
COL1↓,
COL3A1↓,

3371- QC,    Quercetin induces MGMT+ glioblastoma cells apoptosis via dual inhibition of Wnt3a/β-Catenin and Akt/NF-κB signaling pathways
- in-vitro, GBM, T98G
TIMP2↑, MMP2, and MMP9 was significantly decreased by quercetin treatment, while TIMP1 and TIMP2 were upregulated (
TumCG↓, Quercetin significantly suppressed the growth and migration of human GBM T98G cells, induced apoptosis, and arrested cells in the S-phase cell cycle
TumCMig↓,
Apoptosis↑,
TumCCA↑,
MMP↓, collapse of mitochondrial membrane potential, ROS generation, enhanced Bax/Bcl-2 ratio, and strengthened cleaved-Caspase 9 and cleaved-Caspase 3 suggested the involvement of ROS-mediated mitochondria-dependent apoptosis in the process
ROS↑,
Bax:Bcl2↑,
cl‑Casp9↑,
cl‑Casp3↑,
DNAdam↑, quercetin-induced apoptosis was accompanied by intense DNA double-strand breaks (DSBs), γH2AX foci formation, methylation of MGMT promoter, increased cleaved-PARP, and reduced MGMT expression
γH2AX↑,
MGMT↓,
cl‑PARP↑,

3361- QC,    Quercetin ameliorates testosterone secretion disorder by inhibiting endoplasmic reticulum stress through the miR-1306-5p/HSD17B7 axis in diabetic rats
- in-vivo, Nor, NA - in-vitro, NA, NA
*BG↓, Two doses of quercetin increased rat body weight and testicular weight, decreased blood glucose, and inhibited oxidative stress.
*ROS↓,
*SOD↑, Both doses of quercetin reduced reactive oxygen species and malondialdehyde levels, and increased superoxide dismutase level in HG-treated cells.
*MDA↓,
*ER Stress↓, quercetin inhibits endoplasmic reticulum stress
*iNOS↓, Quercetin could eliminate the upregulation of iNOS, ET-1, and AR mRNA levels in HG-treated cells
*CHOP↓, HG treatment increased CHOP and Grp78 mRNA and protein levels in HG-treated cells, and two doses (5 or 10 μM) of quercetin all decreased these levels
*GRP78/BiP↓,
*antiOx↓, Quercetin is a natural polyphenol compound with anti-inflammatory [37], anti-oxidant [38], and blood sugar lowering properties
*Inflam↓,
*JAK2↑, Our results in vitro showed that quercetin treatment upregulated the phosphorylation levels of JAK2 and STAT3 in HG treated cells. (activating of the JAK2/STAT3 pathway could inhibit ER stress)
*STAT3?,

3362- QC,    The effect of quercetin on cervical cancer cells as determined by inducing tumor endoplasmic reticulum stress and apoptosis and its mechanism of action
- in-vitro, Cerv, HeLa
Apoptosis↑, The apoptosis rate in the quercetin group increased significantly in comparison with the blank control group,
cycD1↓, Cyclin D1 showed a tendency to decrease progressively
Casp3↑, Caspase-3, GRP78, and CHOP expression levels in the quercetin intervention group rose significantly in comparison with the blank control group
GRP78/BiP↑,
CHOP↑,
tumCV↓, viability of the cervical cancer HeLe cells was inhibited by quercetin in a dose-dependent manner
IRE1↑, The IRE1, p-Perk, and c-ATF6 levels in the quercetin intervention group (20, 40, and 80 μmol/L) rose gradually in comparison with the blank control group
p‑PERK↑,
c-ATF6↑,
ER Stress↑, quercetin can induce ERS to initiate HeLe cell apoptosis.

3363- QC,    The Protective Effect of Quercetin on Endothelial Cells Injured by Hypoxia and Reoxygenation
- in-vitro, Nor, HBMECs
*Apoptosis↓, Quercetin can promote the viability, migration and angiogenesis of HBMECs, and inhibit the apoptosis.
*angioG↑,
*NRF2↑, quercetin can also activate Keap1/Nrf2 signaling pathway, reduce ATF6/GRP78 protein expression.
*Keap1↓,
*ATF6↓,
*GRP78/BiP↓,
*CLDN5↑, quercetin could increase the expression of Claudin-5 and Zonula occludens-1.
*ZO-1↑,
*MMP↑, reducing mitochondrial membrane potential damage and inhibiting cell apoptosis.
*BBB↑, quercetin can increase the level of BBB connexin, suggesting that quercetin can maintain BBB integrity.
*ROS↓, Quercetin Could Inhibit Oxidative Stress
*ER Stress↓, In our study, ER stress was activated by H/R, and the levels of ATF6 and GRP78 were increased. Quercetin at 1 μmol/L was able to significantly reduce the protein levels of both, inhibit ER stress, and protect HBMECs from H/R injury

3364- QC,    Quercetin Protects Human Thyroid Cells against Cadmium Toxicity
- in-vitro, Nor, NA
*MDA↓, MDA production was increased significantly after incubation with CdCl 2 1 and 10 μM compared with untreated cells (p < 0.001). This effect was significantly attenuated when the cultures were supple‐ mented with quercetin
*GRP78/BiP↓, A significant increase in GRP78 protein expression was detected in Nthy‐ori‐3‐1 cells exposed to 0.1 or 1 μM of CdCl 2 for 2 h compared with untreated cells. Again, this action was reversed by pretreatment with quercetin 5 μM

3365- QC,    Quercetin attenuates sepsis-induced acute lung injury via suppressing oxidative stress-mediated ER stress through activation of SIRT1/AMPK pathways
- in-vivo, Sepsis, NA
*ER Stress↓, quercetin could inhibit the level of ER stress as evidenced by decreased mRNA expression of PDI, CHOP, GRP78, ATF6, PERK, IRE1α
*PDI↓,
*CHOP↓,
*GRP78/BiP↓,
*ATF6↓,
*PERK↓,
*IRE1↓,
*MMP↑, and improve mitochondrial function, as presented by increased MMP, SOD level and reduced production of ROS, MDA.
*SOD↑,
*ROS↓,
*MDA↓,
*SIRT1↑, quercetin upregulated SIRT1/AMPK mRNA expression.
*AMPK↑,
*Sepsis↓, quercetin could protect against sepsis-induced ALI by suppressing oxidative stress-mediated ER stress and mitochondrial dysfunction via induction of the SIRT1/AMPK pathways.

3366- QC,    Quercetin Attenuates Endoplasmic Reticulum Stress and Apoptosis in TNBS-Induced Colitis by Inhibiting the Glucose Regulatory Protein 78 Activation
- in-vivo, IBD, NA
*Apoptosis↓, quercetin improved TNBS-induced histopathological alterations, apoptosis, inflammation, oxidative stress, and ER stress
*Inflam↓,
*ROS↓,
*ER Stress↓, suggests that quercetin has a regulatory effect on ER stress-mediated apoptosis, and thus may be beneficial in treating IBD.
*TNF-α↓, Quercetin reduced the TNF-α and MPO levels associated with colitis
*MPO↓,
*p‑JNK↓, The HSCORE values of p-JNK (p < 0.001), caspase-12 (p < 0.001), and GRP78 (p = 0.004) were lowered in the quercetin group when compared to the colitis group
*Casp12↓,
*GRP78/BiP↓,
*antiOx↑, protective effect of quercetin in IBD, attributed to its antioxidant properties and NF-kB inhibition
*NF-kB↓,

3367- QC,    Targeting Nrf2 signaling pathway by quercetin in the prevention and treatment of neurological disorders: An overview and update on new developments
- Review, Stroke, NA - Review, AD, NA
*NRF2↑, Que enhanced the expression of Nrf2 and inhibited alterations in the shape and death of neurons in the hippocampus.
*neuroP↑,
*motorD↑, Que protected the blood-brain barrier via stimulating Nrf2 in animal stroke, which alleviated ischemic reperfusion and motor dysfunction.
*Inflam↓, (2) By triggering the Nrf2 pathway, Que reduced the neuroinflammation and oxidative damage brought on by TBI in the cortex
*cognitive↑, (3) In an experimental model of AD, Que enhanced cognitive function by decreasing A1-4, antioxidant activity, and Nrf2 levels in the brain.

3368- QC,    The potential anti-cancer effects of quercetin on blood, prostate and lung cancers: An update
- Review, Var, NA
*Inflam↓, quercetin is known for its anti-inflammatory, antioxidant, and anticancer properties.
*antiOx↑,
*AntiCan↑,
Casp3↓, Quercetin increases apoptosis and autophagy in cancer by activating caspase-3, inhibiting the phosphorylation of Akt, mTOR, and ERK, lessening β-catenin, and stabilizing the stabilization of HIF-1α.
p‑Akt↓,
p‑mTOR↓,
p‑ERK↓,
β-catenin/ZEB1↓,
Hif1a↓,
AntiAg↓, Quercetin have revealed an anti-tumor effect by reducing development of blood vessels. I
VEGFR2↓, decrease tumor growth through targeting VEGFR-2-mediated angiogenesis pathway and suppressing the downstream regulatory component AKT in prostate and breast malignancies.
EMT↓, effects of quercetin on inhibition of EMT, angiogenesis, and invasiveness through the epidermal growth factor receptor (EGFR)/VEGFR-2-mediated pathway in breast cancer
EGFR↓,
MMP2↓, MMP2 and MMP9 are two remarkable compounds in metastatic breast cancer (28–30). quercetin on breast cancer cell lines (MDA-MB-231) and showed that after treatment with this flavonoid, the expression of these two proteinases decreased
MMP↓,
TumMeta↓, head and neck (HNSCC), the inhibitory effect of quercetin on the migration of tumor cells has been shown by regulating the expression of MMPs
MMPs↓,
Akt↓, quercetin by inhibiting the Akt activation pathway dependent on Snail, diminishing the expression of N-cadherin, vimentin, and ADAM9 and raising the expression of E-cadherin and proteins
Snail↓,
N-cadherin↓,
Vim↓,
E-cadherin↑,
STAT3↓, inhibiting STAT3 signaling
TGF-β↓, reducing the expression of TGF-β caused by vimentin and N-cadherin, Twist, Snail, and Slug and increasing the expression of E-cadherin in PC-3 cells.
ROS↓, quercetin exerted an anti-proliferative role on HCC cells by lessening intracellular ROS independently of p53 expression
P53↑, increasing the expression of p53 and BAX in hepatocellular carcinoma (HepG2) cell lines through the reduction of PKC, PI3K, and cyclooxygenase (COX-2)
BAX↑,
PKCδ↓,
PI3K↓,
COX2↓,
cFLIP↓, quercetin by inhibiting PI3K/AKT/mTOR and STAT3 pathways, decreasing the expression of cellular proteins such as c-FLIP, cyclin D1, and c-Myc, as well as reducing the production of IL-6 and IL-10 cytokines, leads to the death of PEL cells
cycD1↓,
cMyc↓,
IL6↓,
IL10↓,
Cyt‑c↑, In addition, quercetin induced c-cytochrome-dependent apoptosis and caspase-3 almost exclusively in the HSB2 cell line
TumCCA↑, Exposure of K562 cells to quercetin also significantly raised the cells in the G2/M phase, which reached a maximum peak in 24 hours
DNMTs↓, pathway through DNA demethylation activity, histone deacetylase (HDAC) repression, and H3ac and H4ac enrichment
HDAC↓,
ac‑H3↑,
ac‑H4↑,
Diablo↑, SMAC/DIABLO exhibited activation
Casp3↑, enhanced levels of activated caspase 3, cleaved caspase 9, and PARP1
Casp9↑,
PARP1↑,
eff↑, green tea and quercetin as monotherapy caused the reduction of levels of anti-apoptotic proteins, CDK6, CDK2, CYCLIN D/E/A, BCL-2, BCL-XL, and MCL-1 and an increase in expression of BAX.
PTEN↑, Quercetin upregulates the level of PTEN as a tumor suppressor, which inhibits AKT signaling
VEGF↓, Quercetin had anti-inflammatory and anti-angiogenesis effects, decreasing VGEF-A, NO, iNOS, and COX-2 levels
NO↓,
iNOS↓,
ChemoSen↑, quercetin and chemotherapy can potentiate their effect on the malignant cell
eff↑, combination with hyperthermia, Shen et al. Quercetin is a method used in cancer treatment by heating, and it was found to reduce Doxorubicin hydrochloride resistance in leukemia cell line K562
eff↑, treatment with ellagic acid, luteolin, and curcumin alone showed excellent anticancer effects.
eff↑, co-treatment with quercetin and curcumin led to a reduction of mitochondrial membrane integrity, promotion of cytochrome C release, and apoptosis induction in CML cells
uPA↓, A-549 cells were shown to have reduced mRNA expressions of urokinase plasminogen activator (uPA), Upar, protein expression of CXCR-4, CXCL-12, SDF-1 when quercetin was applied at 20 and 40 mM/ml by real-time PCR.
CXCR4↓,
CXCL12↓,
CLDN2↓, A-549 cells, indicated that quercetin could reduce mRNA and protein expression of Claudin-2 in A-549 cell lines without involving Akt and ERK1/2,
CDK6↓, CDK6, which supports the growth and viability of various cancer cells, was hampered by the dose-dependent manner of quercetin (IC50 dose of QR for A-549 cells is 52.35 ± 2.44 μM).
MMP9↓, quercetin up-regulated the rates of G1 phase cell cycle and cellular apoptotic in both examined cell lines compared with the control group, while it declined the expressions of the PI3K, AKT, MMP-2, and MMP-9 proteins
TSP-1↑, quercetin increased TSP-1 mRNA and protein expression to inhibit angiogenesis,
Ki-67↓, significant reductions in Ki67 and PCNA proliferation markers and cell survival markers in response to quercetin and/or resveratrol.
PCNA↓,
ROS↑, Also, quercetin effectively causes intracellular ROS production and ER stress
ER Stress↑,

3369- QC,    Pharmacological basis and new insights of quercetin action in respect to its anti-cancer effects
- Review, Pca, NA
FAK↓, Quercetin can inhibit HGF-induced melanoma cell migration by inhibiting the activation of c-Met and its downstream Gabl, FAK and PAK [84]
TumCCA↑, stimulation of cell cycle arrest at the G1 stage
p‑pRB↓, mediated through regulation of p21 CDK inhibitor and suppression of pRb phosphorylation resulting in E2F1 sequestering.
CDK2↑, low dose of quercetin has brought minor DNA injury and Chk2 induction
CycB↓, quercetin has a role in the reduction of cyclin B1 and CDK1 levels,
CDK1↓,
EMT↓, quercetin suppresses epithelial to mesenchymal transition (EMT) and cell proliferation through modulation of Sonic Hedgehog signaling pathway
PI3K↓, quercetin on other pathways such as PI3K, MAPK and WNT pathways have also been validated in cervical cancer
MAPK↓,
Wnt↓,
ROS↑, colorectal cancer, quercetin has been shown to suppress carcinogenesis through various mechanisms including affecting cell proliferation, production of reactive oxygen species and expression of miR-21
miR-21↑,
Akt↓, Figure 1 anti-cancer mechanisms
NF-kB↓,
FasL↑,
Bak↑,
BAX↑,
Bcl-2↓,
Casp3↓,
Casp9↑,
P53↑,
p38↑,
MAPK↑,
Cyt‑c↑,
PARP↓,
CHOP↑,
ROS↓,
LDH↑,
GRP78/BiP↑,
ERK↑,
MDA↓,
SOD↑,
GSH↑,
NRF2↑,
VEGF↓,
PDGF↓,
EGF↓,
FGF↓,
TNF-α↓,
TGF-β↓,
VEGFR2↓,
EGFR↓,
FGFR1↓,
mTOR↓,
cMyc↓,
MMPs↓,
LC3B-II↑,
Beclin-1↑,
IL1β↓,
CRP↓,
IL10↓,
COX2↓,
IL6↓,
TLR4↓,
Shh↓,
HER2/EBBR2↓,
NOTCH↓,
DR5↑, quercetin has enhanced DR5 expression in prostate cancer cells
HSP70/HSPA5↓, Quercetin has also suppressed the upsurge of hsp70 expression in prostate cancer cells following heat treatment and enhanced the quantity of subG1 cells
CSCs↓, Quercetin could also suppress cancer stem cell attributes and metastatic aptitude of isolated prostate cancer cells through modulating JNK signaling pathway
angioG↓, Quercetin inhibits angiogenesis-mediated of human prostate cancer cells through negatively modulating angiogenic factors (TGF-β, VEGF, PDGF, EGF, bFGF, Ang-1, Ang-2, MMP-2, and MMP-9)
MMP2↓,
MMP9↓,
IGFBP3↑, Quercetin via increasing the level of IGFBP-3 could induce apoptosis in PC-3 cells
uPA↓, Quercetin through decreasing uPA and uPAR expression and suppressing cell survival protein and Ras/Raf signaling molecules could decrease prostate cancer progression
uPAR↓,
RAS↓,
Raf↓,
TSP-1↑, Quercetin through TSP-1 enhancement could effectively inhibit angiogenesis

3370- QC,    Quercetin downregulates matrix metalloproteinases 2 and 9 proteins expression in prostate cancer cells (PC-3)
- in-vitro, Pca, PC3
MMP2↓, quercetin treatment decreased the expressions of MMP-2 and MMP-9 in dose-dependent manner.
MMP9↓,

3360- QC,    Role of Flavonoids as Epigenetic Modulators in Cancer Prevention and Therapy
- Review, Var, NA
HDAC↓, Quercetin modulates the expression of various chromatin modifiers and declines the activity of HDACs, DNMTs and HMTs in a dose-dependent manner in human cervical cancer (HeLa) cells
DNMTs↓,
HMTs↓,
Let-7↑, Quercetin also induced let-7c which decreased pancreatic tumor growth by posttranscriptional activation of Numbl and indirect inhibition of Notch
NOTCH↓,

3372- QC,  FIS,  KaempF,    Anticancer Potential of Selected Flavonols: Fisetin, Kaempferol, and Quercetin on Head and Neck Cancers
- Review, HNSCC, NA
ROCK1↑, quercetin affects the level of RhoA and NF-κB proteins in SAS cells, and stimulates the expression of RhoA, ROCK1, and NF-κB in SAS cells [53].
TumCCA↓, inhibition of the cell cycle;
HSPs↓, inhibition of heat shock proteins;
RAS↓, inhibition of Ras protein expression.
ROS↑, fisetin induces production of reactive oxygen species (ROS), increases Ca2+ release, and decreases the mitochondrial membrane potential (Ψm) in head and neck neoplastic cells.
Ca+2↑,
MMP↓,
Cyt‑c↑, quercetin increases the expression level of cytochrome c, apoptosis inducing factor and endonuclease G
Endon↑,
MMP9↓, quercetin inhibits MMP-9 and MMP-2 expression and reduces levels of the following proteins: MMP-2, -7, -9 [49,53] and -10
MMP2↓,
MMP7↓,
MMP-10↓,
VEGF↓, as well as VEGF, NF-κB p65, iNOS, COX-2, and uPA, PI3K, IKB-α, IKB-α/β, p-IKKα/β, FAK, SOS1, GRB2, MEKK3 and MEKK7, ERK1/2, p-ERK1/2, JNK1/2, p38, p-p38, c-JUN, and pc-JUN
NF-kB↓,
p65↓,
iNOS↓,
COX2↓,
uPA↓,
PI3K↓,
FAK↓,
MEK↓,
ERK↓,
JNK↓,
p38↓,
cJun↓,
FOXO3↑, Quercetin causes an increase in the level of FOXO1 protein both in a dose- and time-dependent way; however, it does not affect changes in expression of FOXO3a

3373- QC,    The Effect of Quercetin in the Yishen Tongluo Jiedu Recipe on the Development of Prostate Cancer through the Akt1-related CXCL12/ CXCR4 Pathway
- in-vitro, Pca, DU145
TumCP↓, Quercetin inhibited the proliferation of DU145 cells by upregulating caspase-3 and downregulating Bcl-2 expression, promoting apoptosis and reducing invasion and migration abilities.
Casp3↑,
Bcl-2↓,
Apoptosis↑,
TumCI↓,
TumCMig↓,
CXCL12↓, In vivo, quercetin downregulated CXCL12 and CXCR4 expressions and inhibited PCa development by the Akt1-related CXCL12/CXCR4 pathway.
CXCR4↓,

3374- QC,    Therapeutic effects of quercetin in oral cancer therapy: a systematic review of preclinical evidence focused on oxidative damage, apoptosis and anti-metastasis
- Review, Oral, NA - Review, AD, NA
α-SMA↓, In oral cancer cells, quercetin could inhibit EMT via up-regulation of claudin-1 and E-cadherin and down-regulation of α-SMA, vimentin, fibronectin, and Slug [29]
α-SMA↑, OSC20 Invasion: ↓Migration, ↑Expression of epithelial markers (E-cadherin & claudin-1), ↑Expression of mesenchymal markers (fibronectin, vimentin, & α-SMA),
TumCP↓, quercetin significantly reduced cancer cell proliferation, cell viability, tumor volume, invasion, metastasis and migration
tumCV↓,
TumVol↓,
TumCI↓,
TumMeta↓,
TumCMig↓,
ROS↑, This anti-cancer agent induced oxidative stress and apoptosis in the cancer cells.
Apoptosis↑,
BioAv↓, The efficacy of quercetin (as lipophilic) is much impacted by its poor absorption rates, which define its bioavailability. The research on quercetin's bioavailability in animal models shows it may be as low as 10%
*neuroP↑, quercetin has been observed to exhibit neuroprotective effects in Alzheimer's disease through its anti-oxidants, and anti-inflammatory properties and inhibition of amyloid-β (Aβ) fibril formation
*antiOx↑,
*Inflam↓,
*Aβ↓,
*cardioP↑, Additionally, quercetin protects the heart by stopping oxidative stress, inflammation, apoptosis, and protein kinases
MMP↓, ↓MMP, ↑Cytosolic Cyt. C,
Cyt‑c↑,
MMP2↓, ↓Activation MMP-2 & MMP-9, ↓Expression levels of EMT inducers & MMPs, Downregulated Twist & Slug
MMP9↓,
EMT↓,
MMPs↓,
Twist↓,
Slug↓,
Ca+2↑, ↑Apoptosis, ↑ROS, ↑Ca2+ production, ↑Activities of caspase‑3, caspase‑8 & caspase‑9
AIF↑, ↑Mitochondrial release of Cyt. C, AIF, & Endo G
Endon↑,
P-gp↓, ↓ Protein levels of P-gp, & P-gp Expression
LDH↑, ↑LDH release
HK2↓, CAL27 cells) 80µM/24h Molecular markers: ↓Activities of HK, PK, & LDH, ↓Glycolysis, ↓Glucose uptake, ↓Lactate production, ↓Viability, ↓G3BP1, & YWHA2 protein levels
PKA↓,
Glycolysis↓,
GlucoseCon↓,
lactateProd↓,
GRP78/BiP↑, Quercetin controls the activation of intracellular Ca2+ and calpain-1, which then activates GRP78, caspase-12, and C/EBP homologous protein (CHOP) in oral cancer cells
Casp12↑,
CHOP↑,

3375- QC,    Quercetin Mediated TET1 Expression Through MicroRNA-17 Induced Cell Apoptosis in Melanoma Cells
- in-vitro, Melanoma, B16-BL6
TET1↑, Our results suggest that the expression of TET1 was increased following treatment with quercetin in OCM-1, SK-MEL-1, and B16 cells.
TumCI↓, The results showed that the increased expression of TET1-induced apoptosis, increased 5-hydroxymethylcytosine (5 hmC). and inhibited invasion.

3376- QC,    Inhibiting CDK6 Activity by Quercetin Is an Attractive Strategy for Cancer Therapy
- in-vitro, BC, MCF-7 - in-vitro, Lung, A549
CDK6↓, The cell-based protein expression studies in the breast (MCF-7) and lung (A549) cancer cells revealed that the treatment of quercetin decreases the expression of CDK6.
tumCV↓, Quercetin also decreases the viability and colony formation potential of selected cancer cells.
Apoptosis↑, Moreover, quercetin induces apoptosis, by decreasing the production of reactive oxygen species and CDK6 expression
ROS↓,
eff↑, Interestingly, when used in combination, quercetin increases the efficiencies of other anticancer molecules like losartan, paclitaxel, and resveratrol in different cancers

3377- QC,    Quercetin inhibits a large panel of kinases implicated in cancer cell biology
PDGF↓, decreased the activity of 16 kinases by more than 80%, including ABL1, Aurora-A, -B, -C, CLK1, FLT3, JAK3, MET, NEK4, NEK9, PAK3, PIM1, RET, FGF-R2, PDGF-Rα and -Rß.
FLT3↓,
JAK3↓,
MET↓,
RET↓,
FGFR2↓,
other↓, Quercetin markedly inhibited the activity of both the CLK1 and CLK4 kinases at 2 uM but inhibited to a much lower extent the activities of the CLK2 and CLK3 kinases

3378- QC,    CK2 and PI3K are direct molecular targets of quercetin in chronic lymphocytic leukaemia
- in-vitro, AML, NA
CK2↓, We demonstrated that the activity of protein kinase CK2, which positively triggers PI3K/Akt pathway by inactivating PTEN phosphatase, is inhibited by quercetin
PI3K↓, The combined inhibition of CK2 and PI3K kinase activities by quercetin restored ABT-737 sensitivity and increased lethality in human leukemia cells.
TumCD↑,
Akt↓, Quercetin inhibits the PI3K-Akt-Mcl-1 pathway
Mcl-1↓,
PTEN↑, Inhibition of CK2 can rescue PTEN activity increasing apoptosis in CLL

3379- QC,    The Effect of Quercetin Nanosuspension on Prostate Cancer Cell Line LNCaP via Hedgehog Signaling Pathway
- in-vitro, Pca, LNCaP
tumCV↓, The cell viability gradually decreased with increased concentration of quercetin nanoparticles.
HH↓, To sum up, nanoparticles of quercetin improved the inhibitory role in progression of PCa on cell line LNCaP via Hh signaling pathway. targeted inhibition of the Hh pathway could also be an efficient way to stop PCa progression.

3380- QC,    Quercetin as a JAK–STAT inhibitor: a potential role in solid tumors and neurodegenerative diseases
- Review, Var, NA - Review, Park, NA - Review, AD, NA
JAK↓, plant polyphenols, especially quercetin, exert their inhibitory effects on the JAK–STAT pathway through known and unknown mechanisms.
STAT↓,
Inflam↓, quercetin significantly reduced levels of inflammation moderators, including NO synthase, COX-2, and CRP, in a human hepatocyte-derived cell line
NO↓,
COX2↓,
CRP↓,
selectivity↑, , quercetin is not harmful to healthy cells, while it can impose cytotoxic effects on cancer cells through a variety of mechanisms,
*neuroP↑, Alzheimer’s disease because of its antioxidant and anti-inflammatory activity.
STAT3↓, demonstrated as a suppressor of the STAT3 activation signaling pathway
cycD1↓, Rb phosphorylation, cyclin D1 expression, and MMP-2 secretion are inhibited by 48 h treatment with 25 µM quercetin in T98G and U87 GBM cell lines
MMP2↓,
STAT4↓, by inhibiting IL-12-induced tyrosine phosphorylation of STAT3, STAT4, JAK2, and TYK2, quercetin inhibits the proliferation of T cells and differentiation of Th1
JAK2↓,
TumCP↓,
Diff↓,
*eff↑, administration of quercetin with piperine alone and in combination significantly prevented neuroinflammation via reducing the levels of IL-6, TNF-α (two potent activators of the JAK–STAT pathway), and IL-1β in PD in experimental rats
*IL6↓,
*TNF-α↓,
*IL1β↓,
*Aβ↓, quercetin suppressing β-secretase (an enzyme engaged in Aβ formation) and aggregation of Aβ

3381- QC,    Quercetin induces cell death in cervical cancer by reducing O-GlcNAcylation of adenosine monophosphate-activated protein kinase
- in-vitro, Cerv, HeLa
SREBP1↓, quercetin treatment decreased the immunoreactivities of OGT and SREBP-1 in HeLa cells. Our
TumCP↓, Quercetin decreased cell proliferation and induced cell death, but its effect on HaCaT cells was lower than that on HeLa cells.
TumCD↑,
AMPK↑, Quercetin decreased the expression of global O-GlcNAcylation and increased AMPK activation by reducing the O-GlcNAcylation of AMPK
SREBP1↓, Once activated, AMPK regulates various proteins involved in metabolism, which suppress energy consumption and cellular growth, such as sterol regulatory element binding protein 1 (SREBP-1
FASN↓, FAS and ACC were significantly decreased in cells treated with quercetin
ACC↓,

3350- QC,    Quercetin and the mitochondria: A mechanistic view
- Review, NA, NA
*antiOx↑, antioxidant and anti-inflammatory properties
*Inflam↓,
*NRF2↑, Quercetin is able to activate the master regulator nuclear factor erythroid 2-related factor 2 (Nrf2)
ROS⇅, That is, as a free radical-scavenging antioxidant, quercetin protects cells against DNA damage induced by reactiveoxygen species (ROS), but the oxidized quercetin intermediates (see above) can then react with glutathione (GSH) thereby lowering GSH
*NRF2↑, 10uM (24 h) Mouse primary hepatocytes Activation of Nrf2; ↑HO-1 levels; ↑expression of PPARα and PGC-1α
*HO-1↑,
*PPARα↑,
*PGC-1α↑,
*SIRT1↑, Rat hippocampus ↑ SIRT1, PGC-1α, NRF-1, and TFAM levels; ATP levels;
*ATP↑,
ATP↓, L1210 and P388 leukemia cells (Suolinna et al., 1975). At least in part, the authors attributed the pro-apoptotic effect of quercetin in these cell lines to its capacity to inhibit ATP synthase, causing a decrease in ATP content.
ERK↓, downregulation of ERK1/2 by quercetin (50-100 uM for 24 or 48 h, combined or not with resveratrol
cl‑PARP↑, NCaP cells ↑PARP cleavage ↑ Caspase-9, caspase-8, and caspase-3 activities
Casp9↑,
Casp8↑,
BAX↑, MDA-MB-231 cells ↑Bax levels, ↓MMP, ↑cytochrome c release, ↑caspase-9 and caspase-3 activities
MMP↓,
Cyt‑c↑,
Casp3↑,
HSP27↓, T98G cells: ↓Hsp27 and Hsp72 contents, ↓Ras and Raf level
HSP72↓,
RAS↓,
Raf↓,

3339- QC,    Quercetin suppresses ROS production and migration by specifically targeting Rac1 activation in gliomas
- in-vitro, GBM, C6 - in-vitro, GBM, IMR32
BBB↑, capacity to cross the blood–brain barrier
tumCV↓, Quercetin significantly reduced the viability and migration of cells in an ROS-dependent manner with the concomitant inhibition of Rac1/p66Shc expression and ROS production in naïve and Rac1/p66Shc-transfected cell lines, suggestive of preventing Rac
TumCMig↓,
Rac1↓,
p66Shc↓,
ROS↓, treatment of cells with quercetin not only reduced the levels of ROS (Figure 4) but also showed a significant inhibition of p66Shc/Rac1

3340- QC,    Quercetin regulates inflammation, oxidative stress, apoptosis, and mitochondrial structure and function in H9C2 cells by promoting PVT1 expression
- in-vitro, Nor, H9c2
*Inflam↓, Quercetin promotes the proliferation of H9C2 cells, while inhibiting inflammation, oxidative stress, and cell apoptosis, and alleviating the structural and functional dysfunction of mitochondria.
*ROS↓,
*Apoptosis↓,

3341- QC,    Antioxidant Activities of Quercetin and Its Complexes for Medicinal Application
- Review, Var, NA - Review, Stroke, NA
*antiOx↑, we highlight the recent advances in the antioxidant activities, chemical research, and medicinal application of quercetin.
*BioAv↑, Moreover, owing to its high solubility and bioavailability,
*GSH↑, Animal and cell studies found that quercetin induces GSH synthesis
*AChE↓, In this way, it has a stronger inhibitory effect against key enzymes acetylcholinesterase (AChE) and butyrylcholinesterase (BChE), which are associated with oxidative properties
*BChE↓,
*H2O2↓, Quercetin has been shown to alleviate the decline of manganese-induced antioxidant enzyme activity, the increase of AChE activity, hydrogen peroxide generation, and lipid peroxidation levels in rats, thereby preventing manganese poisoning
*lipid-P↓,
*SOD↑, quercetin significantly enhanced the expression levels of endogenous antioxidant enzymes such as Cu/Zn SOD, Mn SOD, catalase (CAT), and GSH peroxidase in the hippocampal CA1 pyramidal neurons of animals suffering from ischemic injury.
*SOD2↑,
*Catalase↑,
*GPx↑,
*neuroP↑, Thus, quercetin may be a potential neuroprotective agent for transient ischemia
*HO-1↑, quercetin can promote fracture healing in smokers by removing free radicals and upregulating the expression of heme-oxygenase- (HO-) 1 and superoxide-dismutase- (SOD-) 1, which protects primary human osteoblasts exposed to cigarette smoke
*cardioP↑, Quercetin has also been shown to prevent heart damage by clearing oxygen-free radicals caused by lipopolysaccharide (LPS)-induced endotoxemia.
*MDA↓, quercetin treatment increased the levels of SOD and CAT and reduced the level of MDA after LPS induction, suggesting that quercetin enhanced the antioxidant defense system
*NF-kB↓, quercetin promotes disease recovery by downregulating the expression of NIK and NF-κB including IKK and RelB, and upregulating the expression of TRAF3.
*IKKα↓,
*ROS↓, quercetin controls the development of atherosclerosis induced by a high-fructose diet by inhibiting ROS and enhancing PI3K/AKT.
*PI3K↑,
*Akt↑,
*hepatoP↑, Quercetin exerts antioxidant and hepatoprotective effects against acute liver injury in mice induced by tertiary butyl hydrogen peroxide. T
P53↑, Quercetin prevents cancer development by upregulating p53, which is the most common inactivated tumor suppressor. It also increases the expression of BAX, a downstream target of p53 and a key pro-apoptotic gene in HepG2 cells
BAX↑,
IGF-1R↓, Studies have found that insulin-like growth factor receptor 1 (IGFIR), AKT, androgen receptor (AR), and cell proliferation and anti-apoptotic proteins are increased in cancer, but quercetin supplementation normalizes their expression
Akt↓,
AR↓,
TumCP↓,
GSH↑, Moreover, quercetin significantly increases antioxidant enzyme levels, including GSH, SOD, and CAT, and inhibits lipid peroxides, thereby preventing skin cancer induced by 7,12-dimethyl Benz
SOD↑,
Catalase↑,
lipid-P↓,
*TNF-α↓, Heart: increases TNF-α, and prevents Ca2+ overload-induced myocardial cell injury
*Ca+2↓,

3342- QC,    Quercetin modulates OTA-induced oxidative stress and redox signalling in HepG2 cells — up regulation of Nrf2 expression and down regulation of NF-κB and COX-2
- in-vitro, Nor, HepG2
*ROS↓, Pre-treatment with quercetin ameliorated ROS and calcium release as well as NF-κB induction and expression
*Ca+2↓,
*NF-kB↓,
*NRF2↑, Quercetin induced Nrf-2 nuclear translocation and expression.
*COX2↓, Quercetin's anti-inflammatory property was exhibited as it down regulated COX-2.
*Inflam↓,

3343- QC,    Quercetin, a Flavonoid with Great Pharmacological Capacity
- Review, Var, NA - Review, AD, NA - Review, Arthritis, NA
*antiOx↑, Quercetin has a potent antioxidant capacity, being able to capture reactive oxygen species (ROS), reactive nitrogen species (RNS), and reactive chlorine species (ROC),which act as reducing agents by chelating transition-metal ions.
*ROS↓, Quercetin is a potent scavenger of reactive oxygen species (ROS), protecting the organism against oxidative stress
*angioG↓,
*Inflam↓, anti-inflammatory properties; the ability to protect low-density lipoprotein (LDL) oxidation, and the ability to inhibit angiogenesis;
*BioAv↓, It is known that the bioavailability of quercetin is usually relatively low (0.17–7 μg/mL), less than 10% of what is consumed, due to its poor water solubility (hydrophobicity), chemical stability, and absorption profile.
*Half-Life↑, their slow elimination since their half-life ranges from 11 to 48 h, which could favor their accumulation in plasma after repeated intakes
*GSH↑, Animal and cell studies have demonstrated that quercetin induces the synthesis of GSH
*SOD↑, increase in the expression of superoxide dismutase (SOD), catalase (CAT), and GSH with quercetin pretreatment
*Catalase↑,
*Nrf1↑, quercetin accomplishes this process involves increasing the activity of the nuclear factor erythroid 2-related factor 2 (NRF2), enhancing its binding to the ARE, reducing its degradation
*BP↓, quercetin has been shown to inhibit ACE activity, reducing blood pressure
*cardioP↑, quercetin has positive effects on cardiovascular diseases
*IL10↓, Under the influence of quercetin, the levels of interleukin 10 (IL-10), IL-1β, and TNF-α were reduced.
*TNF-α↓,
*Aβ↓, quercetin’s ability to modulate the enzyme activity in clearing amyloid-beta (Aβ) plaques, a hallmark of AD pathology.
*GSK‐3β↓, quercetin can inhibit the activity of glycogen synthase kinase 3β,
*tau↓, thus reducing tau aggregation and neurofibrillary tangles in the brain
*neuroP↑,
*Pain↓, quercetin reduces pain and inflammation associated with arthritis
*COX2↓, quercetin included the inhibition of oxidative stress, production of cytokines such as cyclooxygenase-2 (COX-2) and proteoglycan degradation, and activation of the nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) (Nrf2/HO-1)
*NRF2↑,
*HO-1↑,
*IL1β↓, Mechanisms included decreased levels of TNF-α, IL-1β, IL-17, and monocyte chemoattractant protein-1 (MCP-1)
*IL17↓,
*MCP1↓,
PKCδ↓, studies with human leukemia 60 (HL-60) cells report that concentrations between 20 and 30 µM are sufficient to exert an inhibitory effect on cytosolic PKC activity and membrane tyrosine protein kinase (TPK) activity.
ERK↓, 50 µM resulted in the blockade of the extracellular signal-regulated kinases (ERK1/2) pathway
BAX↓, higher doses (75–100 µM) were used, as these doses reduced the expression of proapoptotic factors such as Bcl-2-associated X protein (Bax) and caspases 3 and 9
cMyc↓, induce apoptosis at concentrations of 80 µM and also causes a downregulation of cellular myelocytomatosis (c-myc) and Kirsten RAt sarcoma (K-ras) oncogenes
KRAS↓,
ROS↓, compound’s antioxidative effect changes entirely to a prooxidant effect at high concentrations, which induces selective cytotoxicity
selectivity↑, On the other hand, when noncancerous cells are exposed to quercetin, it exerts cytoprotective effects;
tumCV↓, decrease cell viability in human glioma cultures of the U-118 MG cell line as well as an increase in death by apoptosis and cell arrest at the G2 checkpoint of the cell cycle.
Apoptosis↑,
TumCCA↑,
eff↑, quercetin combined with doxorubicin can induce multinucleation of invasive tumor cells, downregulate P-glycoprotein (P-gp) expression, increase cell sensitivity to doxorubicin,
P-gp↓,
eff↑, resveratrol, quercetin, and catechin can effectively block the cell cycle and reduce cell proliferation in vivo
eff↑, cotreatment with epigallocatechin gallate (EGCG) inhibited catechol-O-methyltransferase (COMT) activity, decreasing COMT protein content and thereby arresting the cell cycle of PC-3 human prostate cancer cells
eff↑, synergistic treatment of tamoxifen and quercetin was also able to inhibit prostate tumor formation by regulating angiogenesis
eff↑, coadministration of 2.5 μM of EGCG, genistein, and quercetin suppressed the cell proliferation of a prostate cancer cell line (CWR22Rv1) by controlling androgen receptor and NAD (P)H: quinone oxidoreductase 1 (NQO1) expression
CycB↓, It can also downregulate cyclin B1 and cyclin-dependent kinase-1 (CDK-1),
CDK1↓,
CDK4↓, quercetin causes a decrease in cyclins D1/Cdk4 and E/Cdk2 and an increase in p21 in vascular smooth muscle cells
CDK2↓,
TOP2↓, quercetin is known to be a potent inhibitor of topoisomerase II (TopoII), a cell cycle-associated enzyme necessary for DNA replication
Cyt‑c↑, quercetin can induce apoptosis (cell death) through caspase-3 and caspase-9 activation, cytochrome c release, and poly ADP ribose polymerase (PARP) cleavage
cl‑PARP↑,
MMP↓, quercetin induces the loss of mitochondrial membrane potential, leading to the activation of the caspase cascade and cleavage of PARP.
HSP70/HSPA5↓, apoptotic effects of quercetin may result from the inhibition of HSP kinases, followed by the downregulation of HSP-70 and HSP-90 protein expression
HSP90↓,
MDM2↓, (MDM2), an onco-protein that promotes p53 destruction, can be inhibited by quercetin
RAS↓, quercetin can prevent Ras proteins from being expressed. In one study, quercetin was found to inhibit the expression of Harvey rat sarcoma (H-Ras), K-Ras, and neuroblastoma rat sarcoma (N-Ras) in human breast cancer cells,
eff↑, there was a substantial difference in EMT markers such as vimentin, N-cadherin, Snail, Slug, Twist, and E-cadherin protein expression in response to AuNPs-Qu-5, inhibiting the migration and invasion of MCF-7 and MDA-MB cells

3344- QC,    Quercetin induced ROS production triggers mitochondrial cell death of human embryonic stem cells
- in-vitro, Nor, hESC
mt-ROS↑, mitochondrial reactive oxygen species (ROS), strongly induced by QC in human embryonic stem cells (hESCs) but not in human dermal fibroblasts (hDFs), were responsible for QC-mediated hESC’s cell death.
selectivity↑,
P53↑, . Increased p53 protein stability and subsequent mitochondrial localization by QC treatment triggered mitochondrial cell death only in hESCs.
ROS⇅, QC acts either as a pro-oxidant to be cytotoxic to cancer cells with active proliferation [8, 10] or as an anti-oxidant [9], depending on the cell models,

3346- QC,    Regulation of the Intracellular ROS Level Is Critical for the Antiproliferative Effect of Quercetin in the Hepatocellular Carcinoma Cell Line HepG2
- in-vitro, Liver, HepG2 - in-vitro, Liver, HUH7
TumCCA↑, can induce the cell cycle arrest and apoptosis of hepatocellular carcinoma (HCC) cells by the stabilization or induction of p53
Apoptosis↑,
P53↑,
TumCP↓, quercetin reduced the proliferation of HepG2 cells significantly, but not Huh7 cells
ROS↓, Interestingly, it was found that quercetin down-regulated the intracellular ROS level of HepG2 cells, but not that of Huh7 cells.
antiOx↑, quercetin is useful for HCC treatment as an antioxidant.
HO-1↑, The expression of p53 and HO-1 was upregulated by quercetin after 12 and 24 h, respectively.
CDK1↓, The expression of p53 and HO-1 was increased but that of CHK1 was decreased in response to the increase in quercetin up to 100 μM.

3347- QC,    Recent Advances in Potential Health Benefits of Quercetin
- Review, Var, NA - Review, AD, NA
*antiOx↑, Its strong antioxidant properties enable it to scavenge free radicals, reduce oxidative stress, and protect against cellular damage.
*ROS↓,
*Inflam?, Quercetin’s anti-inflammatory properties involve inhibiting the production of inflammatory cytokines and enzymes,
TumCP↓, exhibits anticancer effects by inhibiting cancer cell proliferation and inducing apoptosis.
Apoptosis↑,
*cardioP↑, cardiovascular benefits such as lowering blood pressure, reducing cholesterol levels, and improving endothelial function
*BP↓, Quercetin‘s ability to reduce blood pressure was also supported by a different investigation
TumMeta↓, The most important impact of quercetin is its ability to inhibit the spread of certain cancers including those of the breast, cervical, lung, colon, prostate, and liver
MDR1↓, quercetin decreased the expression of genes multidrug resistance protein 1 and NAD(P)H quinone oxidoreductase 1 and sensitized MCF-7 cells to the chemotherapy medication doxorubicin
NADPH↓,
ChemoSen↑,
MMPs↓, Inhibiting CT26 cells’ migration and invasion abilities by inhibiting their expression of tissue inhibitors of metalloproteinases (TIMPs) inhibits their invasion and migration abilities
TIMP2↑,
*NLRP3↓, inhibited NLRP3 by acting on this inflammasome
*IFN-γ↑, quercetin significantly upregulates the gene expression and production of interferon-γ (IFN-γ), which is obtained from T helper cell 1 (Th1), and downregulates IL-4, which is obtained from Th2.
*COX2↓, quercetin is known to decrease the production of inflammatory molecules COX-2, nuclear factor-kappa B (NF-κB), activator protein 1 (AP-1), mitogen-activated protein kinase (MAPK), reactive nitric oxide synthase (NOS), and reactive C-protein (CRP)
*NF-kB↓,
*MAPK↓,
*CRP↓,
*IL6↓, Quercetin suppressed the production of inflammatory cytokines such as IL-6, TNF-α, and IL-1β via upregulating TLR4.
*TNF-α↓,
*IL1β↓,
*TLR4↑,
*PKCδ↓, Quercetin employed suppression on the phosphorylation of PKCδ to control the PKCδ–JNK1/2–c-Jun pathway.
*AP-1↓, This pathway arrested the accumulation of AP-1 transcription factor in the target genes, thereby resulting in reduced ICAM-1 and inflammatory inhabitation
*ICAM-1↓,
*NRF2↑, Quercetin overexpressed Nrf2 and targeted its downstream gene, contributing to increased HO-1 levels responsible for the down-regulation of TNF-α, iNOS, and IL-6
*HO-1↑,
*lipid-P↓, Quercetin acts as a potent antioxidant by scavenging ROS, inhibiting lipid peroxidation, and enhancing the activity of antioxidant enzymes
*neuroP↑, This helps to counteract oxidative stress and protect against neurodegenerative processes that contribute to AD
*eff↑, rats treated with chronic rotenone or 3-nitropropionic acid showed enhanced neuroprotection when quercetin and fish oil were taken orally
*memory↑, Both memory and learning abilities in the test animals increased
*cognitive↑,
*AChE↓, The increase in AChE activity brought on by diabetes was prevented in the cerebral cortex and hippocampus by quercetin at a level of 50 mg/kg body weight.
*BioAv↑, consumption of fried onions compared to black tea, suggesting that the form of quercetin present in onions is better absorbed than that in tea
*BioAv↑, This suggests that dietary fat can increase the absorption of quercetin [180]
*BioAv↑, potential of liposomes to enhance the bioactivity and bioavailability of quercetin has been the subject of several investigations
*BioAv↑, several emulsion types that may be employed to encapsulate quercetin, but oil-in-water (O/W) emulsions are the most widely utilized.
*BioAv↑, the kind of oil (triglyceride oils made up of either long-chain or medium-chain fatty acids) affected the bioaccessibility of quercetin and gastrointestinal stability, emphasizing the significance of picking a suitable oil phase

3348- QC,    Quercetin and iron metabolism: What we know and what we need to know
- Review, NA, NA
*IronCh↑, Quercetin alleviates iron overload induced by various pathologies as a natural iron chelator.
*ROS↓, Quercetin's iron-chelating property and direct scavenging action against ROS (reactive oxygen species) are believed to be the essence of its antioxidant activity.
*AntiAg↑,
*Fenton↓, Cheng and Breen (Cheng and Breen, 2000) found that quercetin suppressed the Fenton reaction by forming a Fe-quercetin-ATP complex.
*lipid-P↓, quercetin effectively decreases iron deposition, and it alleviates lipid peroxidation as well as protein oxidation in the livers, kidneys and hearts of iron-dextran-overloaded mice.
*hepatoP↑, quercetin acts as a reliable liver protector to prevent iron-provoked oxidative damage
*RenoP↑, modulation of iron by quercetin has been shown to prevent glycerol-induced acute myoglobinuric renal failure
HIF-1↑, in both human prostate adenocarcinoma cell lines (LNCaP, DU-145, and PC-3 cell lines) and HeLa cells, quercetin treatment appears to induce HIF-1/2αaccumulation, which may give rise to some undesirable consequences in cases such as cancer treatment
ROS↑, The redox status of quercetin determines whether it can undergo oxido-reductive activation and then be subjected to the iron-involved redox cycling of the Fenton reaction to produce substantial amounts of ROS.

3349- QC,    Quercetin Exerted Protective Effects in a Rat Model of Sepsis via Inhibition of Reactive Oxygen Species (ROS) and Downregulation of High Mobility Group Box 1 (HMGB1) Protein Expression
- in-vivo, Sepsis, NA
*Sepsis↓, results showed that quercetin reduced the tissue edema, congestion, and hemorrhage, increased the alveolar volume, and helped to maintain the lung anatomy of septic rats.
*ROS↓, Admistration of quercetin at the dosage of 15 and 20 mg/kg to septic rats caused significant reduction in the ROS levels.
*SOD↑, The results showed that administration of quercetin at the dosage of 15 and 5 mg/kg to septic rats caused a significant increase in SOD, CAT, and APX expression levels
*Catalase↑,
*HMGB1↓, quercetin caused a significant decrease in HMGB1 protein levels
*Inflam↓, quercetin was found to reduce the inflammation associated with sepsis
*TAC↑, significant increase in the expression of antioxidant enzymes.

3338- QC,    Quercetin: Its Antioxidant Mechanism, Antibacterial Properties and Potential Application in Prevention and Control of Toxipathy
- Review, Var, NA - Review, Stroke, NA
*antiOx↑, The antioxidant mechanism of quercetin in vivo is mainly reflected in its effects on glutathione (GSH), signal transduction pathways, reactive oxygen species (ROS), and enzyme activities.
*GSH↑,
*ROS↓,
*Dose↑, antioxidant properties of quercetin show a concentration dependence in the low dose range but too much of the antioxidant brings about the opposite result
*NADPH↓, quercetin counteracts atherosclerosis by reversing the increased expression of NADPH oxidase i
*AMP↓, decreases in activation of AMP-activated protein kinase, thereby inhibiting NF-κB signaling
*NF-kB↓,
*p38↑, quercetin improves the antioxidant capacity of cells by activating the intracellular p38 MAPK pathway, increasing intracellular GSH levels and providing a source of hydrogen donors in the scavenging of free radical reactions.
*MAPK↑,
*SOD↑, quercetin achieves protection against acute spinal cord injury by up-regulating the activity of SOD, down-regulating the level of malondialdehyde (MDA), and inhibiting the p38MAPK/iNOS signaling pathway
*MDA↓,
*iNOS↓,
*Catalase↑, quercetin reduces imiquimod (IMQ)-induced MDA levels in skin tissues and enhances catalase, SOD, and GSH activities, which together improve the antioxidant properties of the body
*PI3K↑, It also controls the development of atherosclerosis induced by high fructose diet by enhancing PI3K/AKT and inhibiting ROS
*Akt↑,
*lipid-P↓, Quercetin enhances antioxidant activity and inhibits lipid cultivation, and it is effective in the treatment of oxidative liver damag
*memory↑, reversed hypoxia-induced memory impairment
*radioP↑, Quercetin protects cells from radiation and genotoxicity-induced damage by increasing endogenous antioxidant and scavenging free radical levels
*neuroP↑, This suggests that quercetin may be a potential neuroprotective agent against ischemia, which protects CA1 vertebral neurons from I/R injury in the hippocampal region of animals
*MDA↓, quercetin significantly reduced MDA levels and increased SOD and catalase levels.

3351- QC,    Quercetin Exerts Differential Neuroprotective Effects Against H2O2 and Aβ Aggregates in Hippocampal Neurons: the Role of Mitochondria
- Review, AD, NA
*ROS↓, quercetin decreased ROS levels, recovered the normal morphology of mitochondria, and prevented mitochondrial dysfunction in neurons that were treated with H2O2.
*neuroP↑, quercetin exerts differential effects on the prevention of H2O2- and Aβ-induced neurotoxicity in hippocampal neurons

3352- QC,    A review of quercetin: Antioxidant and anticancer properties
- Review, Var, NA
*antiOx↑, Quercetin is considered to be a strong antioxidant due to its ability to scavenge free radicals and bind transition metal ions. T
*lipid-P↓, properties of quercetin allow it to inhibit lipid peroxidation
*TNF-α↓, Quercetin significantly inhibited TNF-α production and gene expression in a dose-dependent manner
*NF-kB↓, inhibiting the activation of NF-κβ,
*COX2↓, Quercetin also inhibits the enzymes cyclooxygenase
*IronCh↑, Quercetin also chelates ions of transition metals such as iron which can initiate the formation of oxygen free radicals
P53↓, Quercetin (248 microM) was found to down regulate expression of mutant p53 protein to nearly undetectable levels in human breast cancer cell lines.
TumCCA↑, Quercetin has been found to arrest human leukemic T-cells in the late G1 phase of the cell cycle.
HSPs↓, Quercetin has been found to inhibit production of heat shock proteins in several malignant cell lines, including breast cancer,[52] leukemia,[53] and colon cancer.[
P21↓, Quercetin (10 microM) has been found to inhibit the expression of the p21-ras oncogene in cultured colon cancer cell lines
RAS↓,
ER(estro)↑, Quercetin has been shown to induce ER II expression in both type I estrogen receptor positive (ER+) and type I estrogen receptor negative (ER-) human breast cancer cells
OS?, Animals treated daily with 40 mg/kg quercetin had a 20-percent increase in life span, while those treated with 160 mg/kg rutin had a 50% increase in life span.

3353- QC,    Quercetin triggers cell apoptosis-associated ROS-mediated cell death and induces S and G2/M-phase cell cycle arrest in KON oral cancer cells
- in-vitro, Oral, KON - in-vitro, Nor, MRC-5
tumCV↓, reduced the vitality of KON cells and had minimal effect on MRC cells.
selectivity↑, Owing to the appropriate dosages of quercetin needed to treat these diseases, normal cells do not exhibit any overtly harmful side effects.
TumCCA↑, quercetin increased the percentage of dead cells and cell cycle arrests in the S and G2/M phases.
TumCMig↓, quercetin inhibited KON cells’ capacity for migration and invasion in addition to their effects on cell stability and structure
TumCI↓,
Apoptosis↑, inducing apoptosis and preventing metastasis, quercetin was found to downregulate the expression of BCL-2/BCL-XL while increasing the expression of BAX.
TumMeta↓,
Bcl-2↓,
BAX↑,
TIMP1↑, TIMP-1 expression was upregulated while MMP-2 and MMP-9 were downregulated.
MMP2↓,
MMP9↓,
*Inflam↓, anti-inflammatory, anti-cancer, antibacterial, antifungal, anti-diabetic, antimalarial, neuroprotective, and cardioprotective properties.
*neuroP↑,
*cardioP↑,
p38↓, MCF-7 cells, quercetin successfully decreased the expression of phosphor p38MAPK, Twist, p21, and Cyclin D1
MAPK↓,
Twist↓,
P21↓,
cycD1↓,
Casp3↑, directly aided by the significant increase in caspase-3 and − 9 levels and activities
Casp9↑,
p‑Akt↓, High quercetin concentrations also caused an inhibition of Akt and ERK phosphorylation
p‑ERK↓,
CD44↓, reduced cell division and triggered apoptosis, albeit to a lesser degree in CD44+/CD24− cells.
CD24↓,
ChemoSen↑, combination of quercetin and doxorubicin caused G2/M arrest in T47D cells, and to a lesser amount in cancer stem cells (CSCs) that were isolate
MMP↓, (lower levels of ΔΨ m), which is followed by the release of Cyto C, AIF, and Endo G from mitochondria, which causes apoptosis and ultimately leads to cell death.
Cyt‑c↑,
AIF↑,
ROS↑, Compared to the control group, quercetin administration significantly raised ROS levels at 25, 50, 100, 200, and 400 µg/mL.
Ca+2↑, increased production of reactive oxygen species and Ca2+, decreased levels of mitochondrial membrane potential (ΔΨ m),
Hif1a↓, Quercetin treatment resulted in a considerable downregulation of HIF-1α, VEGF, MMP2, and MMP9 mRNA and protein expression levels in HOS cells.
VEGF↓,

3354- QC,    Quercetin: Its Main Pharmacological Activity and Potential Application in Clinical Medicine
- Review, Var, NA
*ROS↓, quercetin is the most effective free radical scavenger in the flavonoid family
*IronCh↓, Chelating metal ions: related studies have confirmed that quercetin can induce Cu2+ and Fe2+ to play an antioxidant role through catechol in its structure.
*lipid-P↓, quercetin could inhibit Fe2+-induced lipid peroxidation by binding Fe2+ a
*GSH↑, regulation of glutathione levels to enhance antioxidant capacity.
*NRF2↑, quercetin upregulates the expression of Nrf2 and nuclear transfer by activating the intracellular p38 MAPK pathway, increasing the level of intracellular GSH
TumCCA↑, human leukaemia U937 cells, quercetin induces cell cycle arrest at G2 (late DNA synthesis phase)
ER Stress↑, quercetin can induce ER stress and promote the release of p53, thereby inhibiting the activities of CDK2, cyclin A, and cyclin B, thereby causing MCF-7 breast cancer cells to stagnate in the S phase.
P53↑,
CDK2↓,
cycA1↓,
CycB↓,
cycE↓, downregulation of cyclins E and D, PNCA, and Cdk-2 protein expression and increased expressions of p21 and p27
cycD1↓,
PCNA↓,
P21↑,
p27↑,
PI3K↓, quercetin inhibited the PI3K/AKT/mTOR and STAT3 pathways in PEL, which downregulated the expression of survival cell proteins such as c-FLIP, cyclin D1, and cMyc.
Akt↓,
mTOR↓,
STAT3↓, in excess of 20 μM by inhibiting STAT3 signalling
cFLIP↓,
cMyc↓,
survivin↓, Lung cancer [27] ↓ Survivin ↑DR5
DR5↓,
*Inflam↓, Quercetin has been confirmed to be a long-acting anti-inflammatory substance in flavonoids
*IL6↓, inhibit IL-8 is stronger and can inhibit IL-6 and increase cytosolic calcium levels
*IL8↓,
COX2↓, inhibit the enzymes that produce inflammation (cyclooxygenase (COX) and lipoxygenase (LOX))
5LO↓,
*cardioP↑, The protective mechanism of quercetin on the cardiovascular system
*FASN↓, 25 μM, within 30 minutes could inhibit the synthesis of fatty acids.
*AntiAg↑, quercetin helps reduce lipid peroxidation, platelet aggregation, and capillary permeability
*MDA↓, quercetin can decrease the levels of malondialdehyde (MDA)

3355- QC,    Quercetin exhibits cytotoxicity in cancer cells by inducing two-ended DNA double-strand breaks
- in-vitro, Cerv, HeLa
DNAdam↑, Quercetin induced DNA double-strand break
ROS↑, Reactive oxygen species accumulated in quercetin-treated HeLa cells.
*antiOx↑, antioxidant properties
TOP2↓, Quercetin inhibits Top2 in vitro (Quercetin does not act as a Top2 poison)
γH2AX↑, quercetin concentrations of 50, 100 or 150 μM, γH2AX fluorescence was noticeably observed

3356- QC,    Targeting DNA methyltransferases for cancer therapy
- Review, Var, NA
DNMTs↓, graphical abstract , Quercetin has been shown to downregulate the expression of DNMTs, such as DNMT1 and DNMT3a (ai)

3357- QC,    The polyphenol quercetin induces cell death in leukemia by targeting epigenetic regulators of pro-apoptotic genes
- in-vitro, AML, HL-60 - NA, NA, U937
DNMT1↓, Qu treatment almost eliminates DNMT1 and DNMT3a expression, and this regulation was in part STAT-3 dependent.
DNMT3A↓,
HDAC↓, The treatment also downregulated class I HDACs.
ac‑H3↑, Qu (50 μmol/L) treatment of cell lines for 48 h caused accumulation of acetylated histone 3 and histone 4, resulting in three- to ten fold increases in the promoter region of DAPK1, BCL2L11, BAX, APAF1, BNIP3, and BNIP3L.
ac‑H4↑,
BAX↑,
APAF1↑,
BNIP3↑,
STAT3↑, Quercetin downregulates DNMTs and STAT3

3358- QC,    Effects of quercetin on the DNA methylation pattern in tumor therapy: an updated review
- Review, NA, NA
TET1↑, graphical abstract
DNMTs↓, Here, we review the structure and properties of quercetin, its capacity for DNA methylation modification in tumors

3359- QC,    Quercetin modifies 5′CpG promoter methylation and reactivates various tumor suppressor genes by modulating epigenetic marks in human cervical cancer cells
- in-vitro, Cerv, HeLa
DNMTs↓, When nuclear extracts were incubated with increasing doses of quercetin (25 and 50uM) they were found to inhibit the function of the DNMTs by 32% and 49% respectively, in comparison to untreated control
HDAC↓, quercetin (25 and 50 uM), they were found to inhibit the function of the HDACs by 47% and 62% in comparison to untreated control.
HMTs↓, quercetin (25 and 50 uM), were found to inhibit the function of the HMT H3K9 by 63% and 71%
DNMT3A↓, preferred binding of quercetin on DNMT3A and DNMT3B is within the substrate binding cavity and could competitively inhibit the protein
EZH2↓, Quercetin interacts with EZH2 and functions as an inhibitor
HDAC1↓, Quercetin was able to reduce the activity of class II HDACs significantly, with concomitant downregulation of HDAC1, HDAC2, HDAC6, HDAC7, and HDAC11 expression
HDAC2↓,
HDAC6↓,
HDAC11↓,
G9a↓, quercetin and this correlates well with the observed downregulation of G9A expression
TIMP3↑, Fig8: quercetin resulted in reduced promoter methylation of several TSGs (APC, CDH1, CDH13, DAPK1, FHIT, GSTP1, MGMT, MLH1, PTEN, RARB, RASSF1, SOC51, TIMP3, and VHL
PTEN↑,
SOCS1↑,

68- QC,  BaP,    Differential protein expression of peroxiredoxin I and II by benzo(a)pyrene and quercetin treatment in 22Rv1 and PrEC prostate cell lines
- in-vitro, Pca, 22Rv1 - in-vitro, Pca, PrEC
PrxI∅, Prx-I, Prx-II PrEC cells
PrxII∅, PrEC cells
*toxicity↓, lack of quercetin-mediated changes in Prx expression suggests that quercetin does not interfere with H2O2 levels, and thus may have no deleterious effect in normal prostate cells
ROS↓, <10uM Quercetin
ROS↑, BaP-mediated toxicity in both 22Rv1 and PrEC cells was confirmed by a significant increase in reactive oxygen species
ROS∅, Quercetin also antagonized the increase in ROS by BaP which suggests that BaP-mediated oxidative stress could be blocked with quercetin in 22Rv1 and PrEC cells. S
chemoP↑, Studies have shown that quercetin can be a potential chemopreventative agent in prostate cancer.
PrxII↑, A physiologically achievable concentration (5uM) of quercetin increased the expression of Prx II without affecting the Prx I levels in 22Rv1 cells
i-H2O2↓, Upregulation of Prx II may reduce the intracellular levels of H 2 O2 which in turn can interfere with growth signaling pathways suppressing cell proliferation.

57- QC,    Quercetin inhibits angiogenesis through thrombospondin-1 upregulation to antagonize human prostate cancer PC-3 cell growth in vitro and in vivo
- vitro+vivo, PC, NA
TSP-1↑, protein + mRNA

58- QC,  doxoR,    Quercetin induces cell cycle arrest and apoptosis in CD133+ cancer stem cells of human colorectal HT29 cancer cell line and enhances anticancer effects of doxorubicin
- in-vitro, CRC, HT-29 - in-vitro, NA, CD133+
Bcl-2↓,

59- QC,    Quercetin Inhibits Breast Cancer Stem Cells via Downregulation of Aldehyde Dehydrogenase 1A1 (ALDH1A1), Chemokine Receptor Type 4 (CXCR4), Mucin 1 (MUC1), and Epithelial Cell Adhesion Molecule (EpCAM)
- in-vitro, BC, MDA-MB-231
ALDH1A1↓,
CXCR4↓,
MUC1↓,
EpCAM↓,

60- QC,  EGCG,  isoFl,  isoFl,  isoFl  The dietary bioflavonoid quercetin synergizes with epigallocathechin gallate (EGCG) to inhibit prostate cancer stem cell characteristics, invasion, migration and epithelial-mesenchymal transition
- in-vitro, Pca, pCSCs
Casp3↑,
Casp7↑,
Bcl-2↓,
survivin↓,
XIAP↓,
EMT↓,
Slug↓,
Snail↓,
β-catenin/ZEB1↓,
LEF1↓, LEF-1/TCF

61- QC,    Midkine downregulation increases the efficacy of quercetin on prostate cancer stem cell survival and migration through PI3K/AKT and MAPK/ERK pathway
- in-vitro, Pca, PC3 - in-vitro, Pca, LNCaP - in-vitro, Pca, ARPE-19
p‑PI3K↓, combined therapy inhibited the phosphorylation of PI3K, AKT and ERK1/2, and reduced the protein expression of p38, ABCG2 and NF-κB.
p‑Akt↓,
p‑ERK↓,
NF-kB↓,
p38↓,
ABCG2↓,

62- QC,  GoldNP,    Gold nanoparticles-conjugated quercetin induces apoptosis via inhibition of EGFR/PI3K/Akt-mediated pathway in breast cancer cell lines (MCF-7 and MDA-MB-231)
- in-vitro, BC, MCF-7 - in-vitro, BC, MDA-MB-231
EGFR↓,
PI3k/Akt/mTOR↓, PI3K/Akt/mTOR/GSK-3β
GSK‐3β↓,

63- QC,    Quercetin facilitates cell death and chemosensitivity through RAGE/PI3K/AKT/mTOR axis in human pancreatic cancer cells
- in-vitro, Pca, NA
RAGE↓, Silencing RAGE expression by suppressing the PI3K/AKT/mTOR axis
PI3K↓,
mTOR↓,
Akt↓,
Apoptosis↑,
TumAuto↑,

64- QC,    Quercetin enhances TRAIL-mediated apoptosis in colon cancer cells by inducing the accumulation of death receptors in lipid rafts
- in-vitro, Colon, HT-29 - in-vitro, Colon, SW-620 - in-vitro, Colon, Caco-2
Cyt‑c↑, release of cytochrome c to the cytosol.
BAX↑,
Casp3↑,

65- QC,    Hsp27 participates in the maintenance of breast cancer stem cells through regulation of epithelial-mesenchymal transition and nuclear factor-κB
- in-vitro, BC, NA
HSP27↓,
EMT↓,
NF-kB↓,
Snail↓,
Vim↓,
E-cadherin↑,

66- QC,    Emerging impact of quercetin in the treatment of prostate cancer
- in-vitro, Pca, NA
CycB↓,
CDK1↓,
EMT↓,
PI3K↓,
MAPK↓,
Wnt/(β-catenin)↓, wnt
PSA↓,
VEGF↓,
PARP↑,
Casp3↑,
Casp9↑,
DR5↑,
ROS⇅,
Shh↓,
P53↑,
P21↑,
EGFR↓,

67- QC,  RES,    Overexpression of c-Jun induced by quercetin and resverol inhibits the expression and function of the androgen receptor in human prostate cancer cells
- in-vitro, Pca, LNCaP - in-vitro, Pca, LAPC-4
cJun↑,
AR↓,
NA↓,

56- QC,    Quercetin inhibits epithelial–mesenchymal transition, decreases invasiveness and metastasis, and reverses IL-6 induced epithelial–mesenchymal transition, expression of MMP by inhibiting STAT3 signaling in pancreatic cancer cells
- in-vitro, PC, PANC1 - in-vitro, PC, PATU-8988
EMT↓, quercetin inhibited EMT and decreased the secretion of matrix metalloproteinase (MMP).
MMPs↓,
MMP2↓,
MMP7↓,
STAT3↓,

69- QC,    Quercetin enhances TRAIL-induced apoptosis in prostate cancer cells via increased protein stability of death receptor 5
- in-vitro, Pca, DU145 - in-vitro, Pca, PC3 - in-vitro, Pca, LNCaP
TRAIL↑,
Casp3↑,
Casp9↑,
Casp8↑,
DR5↑,

70- QC,    Quercetin inhibits the expression and function of the androgen receptor in LNCaP prostate cancer cells
- in-vitro, Pca, LNCaP - in-vitro, Pca, LAPC-4
PSA↓, quercetin inhibited the secretion of the prostate-specific, androgen-regulated tumor markers, PSA and hK2
AR↓,
NKX3.1↓,
HK2↓,

71- QC,    Role of Bax in quercetin-induced apoptosis in human prostate cancer cells
- in-vitro, Pca, LNCaP - in-vitro, Pca, PrEC - in-vitro, Pca, YPEN-1 - in-vitro, Pca, HCT116
Casp8↑,
Casp9↑,
PARP↑,
BAD↓,
BAX↑,
PI3K/Akt↓,

72- QC,    Selenium- or quercetin-induced retardation of DNA synthesis in primary prostate cells occurs in the presence of a concomitant reduction in androgen-receptor activity
- in-vitro, Pca, PECs - in-vitro, Pca, LNCaP - in-vitro, Pca, NIH-3T3
AR↓,

73- QC,    The dietary bioflavonoid, quercetin, selectively induces apoptosis of prostate cancer cells by down-regulating the expression of heat shock protein 90
- in-vitro, Pca, LNCaP - in-vitro, Pca, DU145 - in-vitro, Pca, PC3
HSP90↓,
Casp3↑,
Casp9↑,

74- QC,  EGCG,    Prospective randomized trial evaluating blood and prostate tissue concentrations of green tea polyphenols and quercetin in men with prostate cancer
- Human, Pca, NA

75- QC,    Quercetin targets hnRNPA1 to overcome enzalutamide resistance in prostate cancer cells
- in-vitro, Pca, HEK293 - in-vitro, NA, 22Rv1 - in-vitro, NA, C4-2B
hnRNPA1↓,
PSA↓,
NKX3.1↓,
FKBP5↓,
UBE2C↓,
AR-FL↓, FL AR
AR-V7↑,
AR↓,

76- QC,    Multifaceted preventive effects of single agent quercetin on a human prostate adenocarcinoma cell line (PC-3): implications for nutritional transcriptomics and multi-target therapy
- in-vitro, Pca, PC3
aSmase↝,
Diablo↝,
Fas↝,
Hsc70↝,
Hif1a↝,
Mcl-1↝,
HSP90↝,
FLT4↝,
EphB4↝,
DNA-PK↝,
PARP1↝,
ATM↝,
XIAP↝,
PLC↝,
GnT-V↝,
heparanase↝,
NM23↝,
CSR1↝,
SPP1↝,
DNMT1↝,
HDAC4↝,
CXCR4↝,
β-catenin/ZEB1↝,
FBXW7↝,
AMACR↝,
cycD1↝,
IGF-1R↝,
IMPDH1↝,
IMPDH2↝,
HEC1↝,
NHE1↝,
NOS2↝,

77- QC,  EGCG,    The dietary bioflavonoid quercetin synergizes with epigallocathechin gallate (EGCG) to inhibit prostate cancer stem cell characteristics, invasion, migration and epithelial-mesenchymal transition
- in-vitro, Pca, CD44+ - in-vitro, NA, CD133+ - in-vitro, NA, PC3 - in-vitro, NA, LNCaP
Casp3↑,
Casp7↑,
Bcl-2↓,
survivin↓,
XIAP↓,
EMT↓,
Vim↓,
Slug↓,
Snail↓,
β-catenin/ZEB1↓,
LEF1↓, LEF1/TCF
TCF↓, LEF1/TCF
Nanog↓,

78- QC,    Effects of quercetin on insulin-like growth factors (IGFs) and their binding protein-3 (IGFBP-3) secretion and induction of apoptosis in human prostate cancer cells
- in-vitro, Pca, PC3
IGF-1↓,
IGF-2↓,
IGFBP3↑,
Bcl-2↓,
Bcl-xL↓,
Casp3↑,

45- QC,    Quercetin Inhibit Human SW480 Colon Cancer Growth in Association with Inhibition of Cyclin D1 and Survivin Expression through Wnt/β-Catenin Signaling Pathway
- in-vitro, Colon, CX-1 - in-vitro, Colon, SW480 - in-vitro, Colon, HT-29 - in-vitro, Colon, HCT116
cycD1↓,
survivin↓,
Wnt/(β-catenin)↓,

35- QC,    Quercetin may act as a cytotoxic prooxidant after its metabolic activation to semiquinone and quinoidal product
ROS↑,
GSH↓,

36- QC,    Quercetin induces G2 phase arrest and apoptosis with the activation of p53 in an E6 expression-independent manner in HPV-positive human cervical cancer-derived cells
- in-vitro, Cerv, HeLa - in-vitro, Cerv, SiHa
P53↑,
P21↑,
BAX↑,
Casp3↑,
Casp7↑,
TumCCA↑, G2 phase arrest
ROS↑, high concentrations (>40 µM) is able to act as a prooxidant

37- QC,    Low Concentrations of Flavonoids Are Protective in Rat H4IIE Cells Whereas High Concentrations Cause DNA Damage and Apoptosis
- in-vivo, Hepat, H4IIE
DNAdamC↑,
Casp1↑,

38- QC,    Quercetin inhibits prostate cancer by attenuating cell survival and inhibiting anti-apoptotic pathways
- in-vitro, Pca, DU145 - in-vitro, Pca, PC3
ROS↑,
GSH↓,
PI3K/Akt⇅, DU-145↓, PC3↑

39- QC,    A Comprehensive Analysis and Anti-Cancer Activities of Quercetin in ROS-Mediated Cancer and Cancer Stem Cells
- Analysis, NA, NA
ROS↑, production of ROS in both cancer, and cancer stem cells,
GSH↓, By directly reducing the intracellular pool of glutathione (GSH), QC can influence ROS metabolism
IL6↓, QC is its ability to inhibit inflammatory mediators including IFN-γ, IL-6, COX-2, IL-8, iNOS, TNF-α, and many other cancer inflammatory mechanisms
COX2↓,
IL8↓,
iNOS↓,
TNF-α↓,
MAPK↑, quercetin-3-methyl ether stopped the growth of cancer in the esophagus by blocking the Akt/mTOR/P70S6k and MAPK pathways, which are important for the growth of cancer
ERK↑,
SOD↑,
ATP↓,
Casp↑,
PI3K/Akt↓,
mTOR↓,
NOTCH1↓,
Bcl-2↓,
BAX↑,
IFN-γ↓,
TumCP↓, QC directly involves inducing apoptosis and/or the cell cycle arrest process, and also inhibits the propagation of rapidly proliferating cells
TumCCA↑,
Akt↓, quercetin-3-methyl ether stopped the growth of cancer in the esophagus by blocking the Akt/mTOR/P70S6k and MAPK pathways, which are important for the growth of cancer
P70S6K↓,
*Keap1↓,
*GPx↑, inhibiting its negative regulator, Keap1, resulting in Nrf-2 nuclear translocation [86]. This results in the production and activation of enzymes namely GPX, CAT, heme oxygenase 1 (HO-1), peroxiredoxin (PRX)
*Catalase↑,
*HO-1↑,
*NRF2↑,
NRF2↑, The effect of QC on nuclear translocation of Nrf-2 in a time-dependent manner, and increased expression level in HepG2, MgM (malignant mesothelioma) MSTO-211H, and H2452 cells at mRNA and protein quantity has been reported recently
eff↑, quercetin coupled with gold nanoparticles promoted apoptosis by inhibiting the EGFR/P13K/Akt-mediated pathway
HIF-1↓, Quercetin has been shown to suppress the Akt-mTOR pathway and hypoxia-induced factor 1 signaling pathway in gastric cancer cells, resulting in preventative autophagy

40- QC,    Quercetin arrests G2/M phase and induces caspase-dependent cell death in U937 cells
- in-vitro, lymphoma, U937
cycD1↓,
cycE↓,
E2Fs↓,
CycB↑,
Casp↑,

41- QC,    Quercetin induces mitochondrial-derived apoptosis via reactive oxygen species-mediated ERK activation in HL-60 leukemia cells and xenograft
- vitro+vivo, AML, HL-60
Casp8↑,
Casp9↑,
Casp3↑,
ROS↑,
ERK↑,
PARP↑,
MMP↓,

42- QC,    Quercetin induces apoptosis by activating caspase-3 and regulating Bcl-2 and cyclooxygenase-2 pathways in human HL-60 cells
- in-vitro, AML, HL-60
Bcl-2↓, x5.7
BAX↑, x2.9
Casp3↑, x1.1 x1.1
COX2↓, x1.4

43- QC,    Investigation of the anti-cancer effect of quercetin on HepG2 cells in vivo
- in-vivo, Liver, HepG3
cycD1↓,

44- QC,    Preclinical Colorectal Cancer Chemopreventive Efficacy and p53-Modulating Activity of 3′,4′,5′-Trimethoxyflavonol, a Quercetin Analog
- in-vivo, CRC, HCT116
P53↑,

79- QC,    Chemopreventive Effect of Quercetin in MNU and Testosterone Induced Prostate Cancer of Sprague-Dawley Rats
- in-vivo, Pca, NA
GSH↑,
SOD↑,
Catalase↑,
GPx↑,
GSR↑,

46- QC,    Quercetin, but Not Its Glycosidated Conjugate Rutin, Inhibits Azoxymethane-Induced Colorectal Carcinogenesis in F344 Rats
- in-vitro, Colon, F344
β-catenin/ZEB1↓,

47- QC,    Induction of death receptor 5 and suppression of survivin contribute to sensitization of TRAIL-induced cytotoxicity by quercetin in non-small cell lung cancer cells
- in-vitro, NSCLC, H460 - in-vitro, NSCLC, A549
TRAIL↑, cytotoxicity
DR5↑,
survivin↓,

48- QC,    Quercetin Potentiates Apoptosis by Inhibiting Nuclear Factor-kappaB Signaling in H460 Lung Cancer Cells
- in-vitro, NSCLC, H460
TRAILR↑,
Casp10↑,
DFF45↑,
TNFR 1↑,
Fas↑,
NF-kB↓,
IKKα↓,

49- QC,    Plasma rich in quercetin metabolites induces G2/M arrest by upregulating PPAR-γ expression in human A549 lung cancer cells
- in-vitro, Lung, A549
CDK1↓,
CycB↓,
PPARγ↑,

50- QC,    Anticancer effect and mechanism of polymer micelle-encapsulated quercetin on ovarian cancer
- vitro+vivo, Ovarian, A2780S
Casp3↑,
Casp9↑,
Mcl-1↓,
Bcl-2↓,
BAX↑,
angioG↓,

51- QC,    Effect of Quercetin on Cell Cycle and Cyclin Expression in Ovarian Carcinoma and Osteosarcoma Cell Lines
- in-vitro, Ovarian, SKOV3
cycD1↓,

52- QC,    Effect of Quercetin on Cell Cycle and Cyclin Expression in Ovarian Carcinoma and Osteosarcoma Cell Lines
- in-vitro, BC, MCF-7
Bcl-2↓,
BAX↑,
PI3K/Akt↓,

53- QC,    Quercetin regulates β-catenin signaling and reduces the migration of triple negative breast cancer
- in-vitro, BC, NA
E-cadherin↑,
Vim↓,
cycD1↓,
cMyc↓,
EMT↓, tumor cells

54- QC,    Quercetin‑3‑methyl ether suppresses human breast cancer stem cell formation by inhibiting the Notch1 and PI3K/Akt signaling pathways
- in-vitro, BC, MCF-7
EMT↓,
E-cadherin↑,
Vim↓,
MMP2↓,
NOTCH1↓,
PI3K/Akt↓,
PI3k/Akt/mTOR↓,
p‑Akt↓,
EZH2↓, Querectin-3-methyl ether downregulates Notch1, PI3K-AKT and EZH2 signals in breast cancer cells

55- QC,    Quercetin inhibits the growth of human gastric cancer stem cells by inducing mitochondrial-dependent apoptosis through the inhibition of PI3K/Akt signaling
- in-vitro, GC, GCSCs
Bcl-2↓,
BAX↑,
Cyt‑c↑, upregulation of Cyt-c following treatment with quercetin
MMP↓,
PI3K/Akt↓,
Casp3↑,
Casp9↑,

892- QC,    Antioxidant vs. pro-oxidant activities of quercetin in aqueous phase: A Density Functional Theory study
- Analysis, Var, NA
ROS↑, influenced by concentration, pH of environment and the presence of redox metal.

97- QC,  HPT,    Effects of the flavonoid drug Quercetin on the response of human prostate tumours to hyperthermia in vitro and in vivo
- in-vitro, Pca, PC3
HSP72↑,

98- QC,    Quercetin postconditioning attenuates myocardial ischemia/reperfusion injury in rats through the PI3K/Akt pathway
- in-vivo, Stroke, NA
*Bcl-2↑,
*BAX↓,
*Bax:Bcl2↓, Que postconditioning significantly decreased Bax expression and increased Bcl-2 expression
*cardioP↑, cardioprotection by activating the PI3K/Akt signaling pathway and modulating the expression of Bcl-2 and Bax proteins.
*Akt↑,
*PI3K↑,
*LDH↓, Que postconditioning reduced the levels of CK (1642.9±194.3 vs 2679.5±194.3 U/L, P<0.05) and LDH (1273.6±176.5 vs 2618±197.7 U/L, P<0.05) compared to the I/R group

902- QC,    Prooxidant activities of quercetin, p-courmaric acid and their derivatives analysed by quantitative structure–activity relationship
- Analysis, NA, NA
ROS↑, metal ion and concentration of tested phenolics are widely suggested to affect the prooxidant activity of phenolics

100- QC,    Inhibition of Prostate Cancer Cell Colony Formation by the Flavonoid Quercetin Correlates with Modulation of Specific Regulatory Genes
- in-vitro, Pca, PC3 - in-vitro, Pca, DU145 - in-vitro, Pca, LNCaP
cycD1↓, CCND1, CCND2, CCND3
cycE↓, CCNE1, CCNE2
CDK2↓,
CDK4/6↓, CDK4, CDK8
E2Fs↓, E2F2, E2F3
PCNA↓,
cDC2↓,
PTEN↑,
MSH2↑,
P21↑,
EP300↑, p300
BRCA1↑,
NF2↑,
TSC1↑,
TGFβR1↑, TGFβR2
P53↑,
RB1↑, Rb
AKT1↓,
cMyc↓,
CDC7↓,
cycF↓, CCNF
CDC16↓,
CUL4B↑, CUL4B, a member of the cullin gene family that is also known to be involved in control of the cell cycle, was significantly up-regulated by quercetin.
CBP↑,
TSC2↑,
HER2/EBBR2↓, erb-2
BCR↓,

138- QC,  CUR,    Sensitization of androgen refractory prostate cancer cells to anti-androgens through re-expression of epigenetically repressed androgen receptor - Synergistic action of quercetin and curcumin
- in-vitro, Pca, DU145 - in-vitro, Pca, PC3
DNMTs↓,

873- QC,  RES,  CUR,  PI,    Combination Effects of Quercetin, Resveratrol and Curcumin on In Vitro Intestinal Absorption
- in-vitro, Nor, NA
*BioEnh↑, Resveratrol received the greatest enhancement in permeability when combined with other agents: quercetin (310%), curcumin (300%), quercetin and curcumin (323%, 350% with piperine)

889- QC,    The multifaceted role of quercetin derived from its mitochondrial mechanism
- vitro+vivo, Var, NA
MMP↓,
ATP↝,
OXPHOS↝,
ROS↑, a prooxidant effect

890- QC,    PROOXIDANT ACTIVITIES OF ANTIOXIDANTS AND THEIR IMPACT ON HEALTH
- Review, Var, NA
ROS↑, in the presence of the transition metal

891- QC,    Chapter 9 - Quercetin: Prooxidant Effect and Apoptosis in Cancer
- in-vitro, Var, NA
ROS↑, substantial evidence that its prooxidant features are also relevant regarding its tumoricidal effects
AntiTum↑, promote tumoricidal effects.

99- QC,    Quercetin Inhibits Epithelial-to-Mesenchymal Transition (EMT) Process and Promotes Apoptosis in Prostate Cancer via Downregulating lncRNA MALAT1
- in-vitro, Pca, PC3
EMT↓,
E-cadherin↑, Quercetin increased E-cadherin expression and decreased the level of N-cadherin
N-cadherin↓,
Ki-67↓, while the production of Ki67 was significantly reduced by quercetin
PI3K/Akt↓,
MALAT1↓,

893- QC,    Quercetin: Prooxidant Effect and Apoptosis in Cancer
- Analysis, Var, NA
ROS↑, proposal that the capacity of quercetin as a phytochemical that is able to trigger apoptosis in several tumor cell lineages might be related to its prooxidant features.

894- QC,    The antioxidant, rather than prooxidant, activities of quercetin on normal cells: quercetin protects mouse thymocytes from glucose oxidase-mediated apoptosis
- in-vitro, Nor, NA
Apoptosis↑, capable of inducing apoptosis in tumor cell
*NF-kB↓, the G/GO-mediated increase in NF-kB activity was clearly inhibited when the cells were pretreated with 50uM quercetin
*AP-1↓, activation is suppressed by quercetin treatment.
*P53↝, G/GO-mediated oxidative stress activates nuclear translocation and activation of the wild-type p53 in thymocytes and that this activation is inhibited by quercetin.
*ROS↓, normal mouse thymocytes glucose oxidase stress

895- QC,    Theoretical Study of the Antioxidant Activity of Quercetin Oxidation Products
- Analysis, Var, NA
ROS⇅,

896- QC,    Antioxidant and pro-oxidant actions of the plant phenolics quercetin, gossypol and myricetin: Effects on lipid peroxidation, hydroxyl radical generation and bleomycin-dependent damage to DNA
- in-vivo, Var, NA
ROS↑, Hence these naturally-occurring substances can have pro-oxidant effects under some reaction conditions and cannot be classified simplistically as “antioxidants”.

897- QC,    Anti- and prooxidant effects of chronic quercetin administration in rats
- in-vivo, Nor, NA
*MDA↓, in rat livers (decrease was more pronounced in vitamin E-deprived rats)
*GSH↓, in liver
*ROS↑, results suggest that quercetin may act not only as an antioxidant, but also as a prooxidant in rats.

898- QC,    Anti- and pro-oxidant activity of rutin and quercetin derivatives
- Analysis, Var, NA
ROS↑, quercetin derivatives with free catechol moiety or free hydroxyl in position 3 (or both) were pro-oxidant

899- QC,    Intracellular metabolism and bioactivity of quercetin and its in vivo metabolites
- in-vivo, Var, NA
ROS↑, effects of quercetin on cells seem to be dependent both on cell type and in particular on the concentration of quercetin
GSH↓,

900- QC,    Quercetin Affects Erythropoiesis and Heart Mitochondrial Function in Mice
- in-vivo, Nor, NA
*Weight↓, overall weight
*TAC∅, no significant decrease
*ROS↑, working hypothesis is that quercetin interferes with mitochondrial function exacerbating mitochondrial ROS generation and altering the physiology of tissues highly dependent on iron metabolism

901- QC,    Antioxidant/prooxidant effects of α-tocopherol, quercetin and isorhamnetin on linoleic acid peroxidation induced by Cu(II) and H2O2
- Analysis, Var, NA
ROS↑, presence/ absence of metal ions modulates the biological or pharmacological behavior of flavonoids to act as an antioxidant or prooxidant

91- QC,    The roles of endoplasmic reticulum stress and mitochondrial apoptotic signaling pathway in quercetin-mediated cell death of human prostate cancer PC-3 cells
- in-vitro, Pca, PC3
CDK2↓,
cycE↓,
cycD1↓, proteins
ATFs↑,
GRP78/BiP↑,
Bcl-2↓,
BAX↑,
Casp3↑,
Casp8↑,
Casp9↑,
ER Stress↑, stress
CHOP↑,

80- QC,    Quercetin reverses EGF-induced epithelial to mesenchymal transition and invasiveness in prostate cancer (PC-3) cell line via EGFR/PI3K/Akt pathway
- in-vitro, Pca, PC3
Vim↓,
ERK↓,
Snail↓,
Slug↓,
Twist↓,
EGFR↓,
p‑Akt↓,
EGFR↓,
N-cadherin↓,

81- QC,  EGCG,    Enhanced inhibition of prostate cancer xenograft tumor growth by combining quercetin and green tea
- in-vivo, Pca, NA
COMT↓,
MRP1↓,
Ki-67↓,
Bax:Bcl2↑,
AR↓,
Akt↓,
p‑ERK↓, ERK1/2
COMT↓,
eff↑, Enhanced inhibition of prostate cancer xenograft tumor growth by combining quercetin and green tea

82- QC,  AG,    Arctigenin in combination with quercetin synergistically enhances the anti-proliferative effect in prostate cancer cells
- in-vitro, Pca, NA
AR↓,
PI3K/Akt↓,
miR-21↓,
STAT3↓,
BAD↓,
PRAS40↓,
GSK‐3β↓,
PSA↓,
NKX3.1↑,
Bax:Bcl2↑,
miR-19b↓,
miR-148a↓,
AMPKα↓,

83- QC,    Quercetin induces p53-independent apoptosis in human prostate cancer cells by modulating Bcl-2-related proteins: a possible mediation by IGFBP-3
- in-vitro, Pca, PC3
Bcl-2↓,
Bcl-xL↓,
BAX↑,
IGFBP3↑,

84- QC,    Quercetin-induced growth inhibition and cell death in prostatic carcinoma cells (PC-3) are associated with increase in p21 and hypophosphorylated retinoblastoma proteins expression
- in-vitro, Pca, PC3
P21↑,
cDC2↓, Cdc2/Cdk-1
CDK1↓, Cdc2/Cdk-1
CycB↓,
Casp3↑,
Bcl-2↓,
Bcl-xL↓,
BAX↑,
pRB↓,

85- QC,    Quercetin inhibits invasion, migration and signalling molecules involved in cell survival and proliferation of prostate cancer cell line (PC-3)
- in-vitro, Pca, PC3
uPA↓,
uPAR↓,
EGFR↓,
NRAS↓,
Jun↓,
NF-kB↓,
β-catenin/ZEB1↓,
p38↑,
MAPK↑,
cJun↓,
cFos↓,
Raf↓, Raf-1

86- QC,    Quercetin regulates insulin like growth factor signaling and induces intrinsic and extrinsic pathway mediated apoptosis in androgen independent prostate cancer cells (PC-3)
- in-vitro, Pca, PC3
BAD↑,
IGFBP3↑,
Cyt‑c↑, Quercetin significantly increases the proapoptotic mRNA levels of Bad, IGFBP-3 and protein levels of Bad, cytochrome C, cleaved caspase-9, caspase-10, cleaved PARP and caspase-3 activity in PC-3 cells
cl‑Casp9↑, cleaved
Casp10↑,
cl‑PARP↑, cleaved
Casp3↑,
IGF-1R↓,
PI3K↓,
p‑Akt↓,
cycD1↓, protein
IGF-1↓, mRNA levels of IGF-1,IGR-2, IGF-1R
IGF-2↓,
IGF-1R↓,

87- QC,    Quercetin inhibits prostate cancer by attenuating cell survival and inhibiting anti-apoptotic pathways
- in-vitro, Pca, LNCaP - in-vitro, Pca, DU145 - in-vitro, Pca, PC3
ROS⇅,
BAX↑, quercetin treatment increased BAX levels
PUMA⇅,
β-catenin/ZEB1↓,
Shc↓,
TAp63α↑, DU-145
MAPK↑, DU-145 DU-145
p‑p42↑,
p‑p44↑,
BIM↑, . In androgen-independent PCa cells with mutated p53 (DU-145), quercetin treatment increases cellular BAX levels whereas PUMA and BIM increased

88- QC,  PacT,    Quercetin Enhanced Paclitaxel Therapeutic Effects Towards PC-3 Prostate Cancer Through ER Stress Induction and ROS Production
- vitro+vivo, Pca, PC3
ROS↑,
ER Stress↑,

89- QC,  doxoR,    Quercetin reverses the doxorubicin resistance of prostate cancer cells by downregulating the expression of c-met
- in-vitro, Pca, PC3
PI3K/Akt↓,
cMET↓,
Casp3↑,
Casp9↑,
MMP↓,

90- QC,  HP,    Combination of quercetin and hyperoside inhibits prostate cancer cell growth and metastasis via regulation of microRNA‑21
- in-vitro, Pca, PC3
ROS↑,
cl‑Casp3↑, cleaved
cl‑PARP↑, cleaved
miR-21↓,
PDCD4↑,

92- QC,    Quercetin Inhibits Angiogenesis Mediated Human Prostate Tumor Growth by Targeting VEGFR- 2 Regulated AKT/mTOR/P70S6K Signaling Pathways
- vitro+vivo, Pca, HUVECs - vitro+vivo, Pca, PC3
VEGF↓, VEGF-R2
HemoG↓,
Akt↓, AKT/mTOR/P70S6K↓
mTOR↓,
P70S6K↓,

93- QC,    Chemical Proteomics Identifies Heterogeneous Nuclear Ribonucleoprotein (hnRNP) A1 as the Molecular Target of Quercetin in Its Anti-cancer Effects in PC-3 Cells
- in-vitro, Pca, PC3
hnRNPA1↓,
Casp3↑, activated
Casp7↑, activated

94- QC,  HPT,    Effects of quercetin on the heat-induced cytotoxicity of prostate cancer cells
- in-vitro, Pca, LNCaP - in-vitro, Pca, PC3 - in-vitro, Pca, JCA-1
HSP70/HSPA5↓,

95- QC,    Quercetin, a natural dietary flavonoid, acts as a chemopreventive agent
- in-vitro, Pca, PC3
p‑ERK↓, ERK1/2
p‑STAT3↓, pSTAT3
p‑Akt↓,
N-cadherin↓,
Vim↓,
cycD1↓,
Snail↓,
Slug↓,
Twist↓, mRNA
PCNA↓,

96- QC,  docx,    Quercetin reverses docetaxel resistance in prostate cancer via androgen receptor and PI3K/Akt signaling pathways
- vitro+vivo, Pca, LNCaP - in-vitro, Pca, PC3
PI3K/Akt↓,
Ki-67↓,
BAX↑,
Bcl-2↓,
EpCAM↓,
Twist↓, Twist2
E-cadherin↑,
P-gp↓,

871- RES,  CUR,  QC,    The effect of resveratrol, curcumin and quercetin combination on immuno-suppression of tumor microenvironment for breast tumor-bearing mice
- in-vitro, BC, 4T1 - in-vivo, BC, 4T1
T-Cell↑, in tumor microenviroment
Neut↓,
Macrophages↓,
ROS↑, RCQ significantly increased reactive oxygen species
MMP↓, in cancer cells
other↓, alleviate immunosuppression of the tumor microenvironment to enhance the anti-tumor effect.
AntiTum↑, at least nearly 5 times higher than that of a single Res/Cur/Que  = 1:1:0.5
TumVol↓, 35-47% tumor inhibition rate

105- RES,  QC,    The Effect of Resveratrol and Quercetin on Epithelial-Mesenchymal Transition in Pancreatic Cancer Stem Cell
- in-vitro, Pca, CD133+
N-cadherin↓,
TNF-α↓,
ACTA2↓,

104- RES,  QC,    Resveratrol and Quercetin in Combination Have Anticancer Activity in Colon Cancer Cells and Repress Oncogenic microRNA-27a
- in-vitro, Colon, HT-29
Casp3↑, x2
PARP↑,
survivin↓,
miR-27a-3p↓, miR-27a
Sp1/3/4↓,
ZBTB10↑,

103- RES,  CUR,  QC,    The effect of resveratrol, curcumin and quercetin combination on immuno-suppression of tumor microenvironment for breast tumor-bearing mice
- vitro+vivo, BC, 4T1
ROS↑,
MMP↓,
Bcl-2↓,
BAX↑,
Casp9↑,
T-Cell↑, (CD4+CD8+)
TGF-β↓,

380- SNP,  QC,  CA,  Chit,    Quercetin- and caffeic acid-functionalized chitosan-capped colloidal silver nanoparticles: one-pot synthesis, characterization, and anticancer and antibacterial activities
- in-vitro, MG, U118MG
TumCG↓, cell viability has constantly decreased by increasing the concentration

1309- TQ,  QC,    Thymoquinone and quercetin induce enhanced apoptosis in non-small cell lung cancer in combination through the Bax/Bcl2 cascade
- in-vitro, Lung, NA
Bcl-2↓,
BAX↑,
Apoptosis↑,

114- VitC,  QC,    Chemoprevention of prostate cancer cells by vitamin C plus quercetin: role of Nrf2 in inducing oxidative stress
- in-vitro, Pca, PC3 - in-vitro, NA, DU145
GPx↓,
GSR↓,
NQO1↓,
NRF2↓,
ROS↑,

3108- VitC,  QC,    The role of quercetin and vitamin C in Nrf2-dependent oxidative stress production in breast cancer cells
- in-vitro, BC, MDA-MB-231 - in-vitro, Lung, A549
NRF2↓, significant decrease in the expression of Nrf2 mRNA and protein levels following the treatment of breast cancer cells with VC and Q
HO-1↓, In the MDA-MB 231 and MCF-7 cell lines, HO1 was significantly suppressed following treatment with VC and Q
ROS↑, It was demonstrated that ROS levels significantly increased in tumor cells treated with VC and Q.
NRF2⇅, it was demonstrated that treatment of MDA-MB 231 cells with 25 µM Q increased the expression of Nrf2, while 50 and 75 µM Q decreased the mRNA levels of Nrf2.


* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 180

Results for Effect on Cancer/Diseased Cells:
5LO↓,1,   ABCG2↓,1,   ACC↓,1,   ACTA2↓,1,   AIF↑,2,   Akt↓,13,   p‑Akt↓,7,   AKT1↓,1,   ALDH1A1↓,1,   AMACR↝,1,   AMPK↑,1,   AMPKα↓,1,   AMPKα↑,2,   angioG↓,3,   AntiAg↓,1,   AntiCan↑,2,   antiOx↑,1,   AntiTum↑,3,   APAF1↑,1,   Apoptosis↓,1,   Apoptosis↑,19,   AR↓,7,   AR-FL↓,1,   AR-V7↑,1,   ASK1↑,1,   aSmase↝,1,   c-ATF6↑,1,   ATFs↑,1,   ATM↝,1,   ATP↓,3,   ATP↝,1,   BAD↓,3,   BAD↑,1,   Bak↑,1,   BAX↓,1,   BAX↑,22,   Bax:Bcl2↑,4,   BBB↑,1,   Bcl-2↓,19,   Bcl-xL↓,3,   BCR↓,1,   Beclin-1↑,1,   BIM↑,1,   BioAv↓,1,   BioEnh↑,7,   BNIP3↑,1,   BRCA1↑,1,   Ca+2↑,4,   Ca+2↝,1,   cardioP↑,1,   Casp↑,2,   Casp1↑,1,   Casp10↑,3,   Casp12↑,1,   Casp3↓,2,   Casp3↑,26,   cl‑Casp3↑,2,   Casp7↑,5,   Casp8↑,7,   Casp9↑,16,   cl‑Casp9↑,2,   Catalase↑,2,   CBP↑,1,   CD24↓,1,   CD44↓,1,   CDC16↓,1,   cDC2↓,2,   CDC7↓,1,   CDK1↓,7,   CDK2↓,4,   CDK2↑,1,   CDK4↓,1,   CDK4/6↓,1,   CDK6↓,2,   cFLIP↓,5,   cFos↓,1,   chemoP↑,2,   ChemoSen↑,5,   Chk2↑,1,   CHOP↓,1,   CHOP↑,5,   cJun↓,2,   cJun↑,1,   CK2↓,1,   CLDN2↓,1,   cMET↓,1,   cMyc↓,8,   COL1↓,1,   COL3A1↓,1,   COMT↓,4,   COX2↓,10,   CRP↓,3,   CSCs↓,2,   CSR1↝,1,   CUL4B↑,1,   CXCL12↓,2,   CXCR4↓,3,   CXCR4↝,1,   cycA1↓,1,   CycB↓,7,   CycB↑,1,   cycD1↓,16,   cycD1↝,1,   cycE↓,4,   cycF↓,1,   CYP19↓,1,   Cyt‑c↑,10,   DFF45↑,2,   Diablo↑,1,   Diablo↝,1,   Diff↓,1,   DNA-PK↝,1,   DNAdam↑,3,   DNAdamC↑,1,   DNMT1↓,1,   DNMT1↝,1,   DNMT3A↓,2,   DNMTs↓,6,   DR5↓,1,   DR5↑,6,   E-cadherin↓,1,   E-cadherin↑,6,   E2Fs↓,2,   ECAR↓,1,   eff↓,2,   eff↑,15,   EGF↓,1,   EGFR↓,9,   p‑eIF2α↓,1,   EMT↓,12,   Endon↑,2,   EP300↑,1,   EpCAM↓,2,   EphB4↝,1,   ER Stress↑,6,   ER(estro)↑,1,   ERK↓,4,   ERK↑,3,   ERK↝,1,   p‑ERK↓,5,   EZH2↓,2,   FAK↓,2,   FAO↓,1,   Fas↑,2,   Fas↝,1,   FasL↑,1,   FASN↓,1,   FBXW7↝,1,   FGF↓,2,   FGFR1↓,1,   FGFR2↓,1,   FKBP5↓,1,   FLT3↓,1,   FLT4↝,1,   FOXO3↑,1,   G9a↓,1,   GlucoseCon↓,5,   GLUT1↓,4,   Glycolysis↓,7,   GnT-V↝,1,   GPx↓,1,   GPx↑,1,   GRP78/BiP↑,5,   GSH↓,9,   GSH↑,3,   GSH∅,1,   GSK‐3β↓,3,   GSR↓,1,   GSR↑,1,   H2O2↑,2,   i-H2O2↓,1,   ac‑H3↑,2,   ac‑H4↑,2,   HDAC↓,4,   HDAC1↓,1,   HDAC11↓,1,   HDAC2↓,1,   HDAC4↝,1,   HDAC6↓,1,   HEC1↝,1,   HemoG↓,1,   heparanase↝,1,   hepatoP↑,1,   HER2/EBBR2↓,2,   HH↓,1,   HIF-1↓,1,   HIF-1↑,1,   Hif1a↓,5,   Hif1a↝,1,   HK2↓,6,   HMTs↓,2,   hnRNPA1↓,2,   HO-1↓,1,   HO-1↑,2,   Hsc70↝,1,   HSP27↓,3,   HSP70/HSPA5↓,3,   HSP72↓,1,   HSP72↑,1,   HSP90↓,2,   HSP90↝,1,   HSPs↓,2,   IFN-γ↓,2,   IGF-1↓,2,   IGF-1R↓,3,   IGF-1R↝,1,   IGF-2↓,2,   IGFBP3↑,4,   IKKα↓,2,   IL10↓,4,   IL1β↓,1,   IL6↓,6,   IL8↓,2,   IMPDH1↝,1,   IMPDH2↝,1,   Inflam↓,2,   iNOS↓,4,   IRE1↑,1,   p‑IRE1↓,1,   IκB↓,1,   JAK↓,1,   JAK2↓,1,   JAK3↓,1,   JNK↓,1,   p‑JNK↓,1,   Jun↓,1,   Ki-67↓,5,   KRAS↓,1,   lactateProd↓,7,   LC3B-II↑,2,   LDH↑,2,   LDHA↓,3,   LEF1↓,3,   Let-7↑,1,   lipid-P↓,1,   Macrophages↓,1,   MALAT1↓,1,   MAPK↓,3,   MAPK↑,4,   MAPK↝,1,   Mcl-1↓,2,   Mcl-1↝,1,   MDA↓,1,   MDM2↓,1,   MDR1↓,1,   MEK↓,1,   MET↓,1,   MGMT↓,1,   miR-148a↓,1,   miR-19b↓,1,   miR-21↓,2,   miR-21↑,1,   miR-27a-3p↓,1,   mitResp↓,1,   MMP↓,15,   MMP-10↓,1,   MMP2↓,13,   MMP3↓,1,   MMP7↓,3,   MMP9↓,8,   MMP9:TIMP1↓,1,   MMPs↓,7,   MRP1↓,1,   MSH2↑,1,   mTOR↓,11,   p‑mTOR↓,1,   MUC1↓,1,   N-cadherin↓,5,   NA↓,1,   NADPH↓,1,   Nanog↓,1,   Neut↓,1,   NF-kB↓,8,   NF2↑,1,   NHE1↝,1,   NKX3.1↓,2,   NKX3.1↑,1,   NM23↝,1,   NO↓,2,   NOS2↝,1,   NOTCH↓,2,   NOTCH1↓,3,   NQO1↓,1,   NQO1↑,1,   NQO2↑,1,   NRAS↓,1,   NRF2↓,2,   NRF2↑,2,   NRF2⇅,1,   OCR↓,1,   OS?,1,   OS↑,2,   other↓,4,   other↑,2,   OXPHOS↝,1,   P-gp↓,5,   P21↓,2,   P21↑,6,   p27↑,1,   p38↓,3,   p38↑,3,   p‑p42↑,1,   p‑p44↑,1,   P450↓,1,   P53↓,1,   P53↑,14,   p65↓,1,   p66Shc↓,1,   P70S6K↓,2,   PARP↓,1,   PARP↑,5,   cl‑PARP↑,6,   PARP1↑,1,   PARP1↝,1,   PCNA↓,4,   PDCD4↑,1,   PDGF↓,2,   PDK3↓,1,   p‑PERK↑,1,   PFKP?,1,   PI3K↓,10,   p‑PI3K↓,1,   PI3K/Akt↓,9,   PI3K/Akt⇅,1,   PI3k/Akt/mTOR↓,3,   PKA↓,1,   PKCδ↓,2,   PKM2↓,4,   PLC↝,1,   PPARγ↑,1,   PRAS40↓,1,   pRB↓,1,   p‑pRB↓,1,   PrxI∅,1,   PrxII↑,1,   PrxII∅,1,   PSA↓,4,   PTEN↑,4,   PUMA⇅,1,   Rac1↓,1,   RadioS↑,1,   Raf↓,3,   RAGE↓,2,   RAS↓,5,   RB1↑,1,   p‑RB1↓,1,   RET↓,1,   Risk↓,1,   ROCK1↑,1,   ROS↓,8,   ROS↑,47,   ROS⇅,6,   ROS∅,2,   mt-ROS↑,1,   SCF↓,1,   selectivity↑,5,   SESN2↑,1,   Shc↓,1,   Shh↓,2,   Slug↓,6,   Snail↓,7,   SOCS1↑,1,   SOD↑,4,   Sp1/3/4↓,2,   SPP1↝,1,   SREBP1↓,2,   STAT↓,1,   STAT3↓,7,   STAT3↑,1,   p‑STAT3↓,2,   STAT4↓,1,   survivin↓,7,   T-Cell↑,2,   TAp63α↑,1,   TCF↓,1,   TET1↑,2,   TGF-β↓,5,   TGFβR1↑,1,   TIMP1↑,1,   TIMP2↑,2,   TIMP3↑,1,   TLR4↓,1,   TNF-α↓,6,   TNFR 1↑,2,   TOP2↓,2,   TRAIL↑,3,   TRAILR↑,2,   TrxR↓,1,   TSC1↑,1,   TSC2↑,1,   TSP-1↑,4,   TumAuto↑,4,   TumCCA↓,1,   TumCCA↑,16,   TumCD↑,2,   TumCG↓,5,   TumCI↓,5,   TumCMig↓,5,   TumCP↓,10,   tumCV↓,9,   TumMeta↓,6,   TumVol↓,4,   Twist↓,5,   UBE2C↓,1,   uPA↓,4,   uPAR↓,2,   VEGF↓,10,   VEGFR2↓,2,   Vim↓,8,   Wnt↓,1,   Wnt/(β-catenin)↓,3,   XIAP↓,3,   XIAP↝,1,   ZBTB10↑,1,   α-SMA↓,1,   α-SMA↑,1,   β-catenin/ZEB1↓,8,   β-catenin/ZEB1↝,1,   γH2AX↑,2,  
Total Targets: 419

Results for Effect on Normal Cells:
AChE↓,3,   Akt↑,3,   ALAT↓,1,   ALDOA↑,1,   AMP↓,1,   AMPK↑,2,   angioG↓,1,   angioG↑,1,   AntiAg↑,2,   AntiCan↑,1,   antiOx↓,2,   antiOx↑,14,   AP-1↓,2,   Apoptosis↓,4,   AST↓,1,   ATF6↓,2,   ATP↑,2,   Aβ↓,4,   BAX↓,1,   Bax:Bcl2↓,1,   BBB↓,1,   BBB↑,1,   BChE↓,1,   Bcl-2↑,1,   BG↓,1,   BioAv↓,2,   BioAv↑,7,   BioEnh↑,3,   BP↓,2,   Ca+2↓,2,   cardioP↑,8,   Casp12↓,1,   Catalase↑,6,   CHOP↓,2,   CLDN5↑,1,   cognitive↑,3,   Copper↓,1,   COX2↓,6,   CRP↓,1,   CXCL1↓,1,   Dose↑,1,   eff↑,2,   eff↝,1,   ER Stress↓,5,   FASN↓,1,   Fenton↓,1,   GlucoseCon↓,1,   Glycolysis↓,1,   GPI↑,1,   GPx↑,3,   GRP58↓,1,   GRP78/BiP↓,5,   GSH↓,2,   GSH↑,4,   GSK‐3β↓,1,   H2O2↓,1,   Half-Life↑,2,   hepatoP↑,3,   Hif1a↑,2,   HK2↓,1,   HK2↑,1,   HMGB1↓,2,   HO-1↑,6,   ICAM-1↓,1,   IFN-γ↑,1,   IKKα↓,1,   IL10↓,1,   IL17↓,1,   IL1β↓,4,   IL6↓,5,   IL8↓,1,   Inflam?,1,   Inflam↓,18,   iNOS↓,4,   IRE1↓,1,   Iron↓,1,   IronCh↓,1,   IronCh↑,2,   JAK2↑,1,   p‑JNK↓,1,   Keap1↓,2,   lactateProd↓,1,   LDH↓,1,   LDHA↑,1,   lipid-P↓,7,   MAPK↓,1,   MAPK↑,1,   MCP1↓,1,   MDA↓,10,   memory↑,3,   MMP↑,4,   motorD↑,1,   MPO↓,1,   NADPH↓,2,   neuroP↑,10,   NF-kB↓,10,   NLRP3↓,3,   NO↓,1,   NOX4↓,1,   Nrf1↑,1,   NRF2↑,10,   p38↑,1,   P53↝,1,   p65↓,1,   Pain↓,1,   PDI↓,1,   PERK↓,1,   PFKL↑,1,   PFKP↓,1,   PGC-1α↑,1,   PI3K↑,3,   PKCδ↓,1,   PKM1↑,1,   PKM2↓,3,   PPARα↑,1,   radioP↑,1,   RenoP↑,1,   ROS↓,21,   ROS↑,2,   Sepsis↓,3,   SIRT1↓,1,   SIRT1↑,4,   SOD↑,7,   SOD2↑,1,   STAT3?,1,   TAC↑,1,   TAC∅,1,   tau↓,1,   p‑tau↓,1,   TLR4↑,1,   TNF-α↓,7,   toxicity↓,1,   UPR↓,1,   Weight↓,1,   XBP-1↓,1,   ZO-1↑,1,  
Total Targets: 136

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:140  Target#:%  State#:%  Dir#:%
  wNotes=on  sortOrder:rid,rpid

 

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