Quercetin Cancer Research Results

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), 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">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

Rank Pathway / Axis Cancer Cells Normal Cells Label Primary Interpretation Notes
1 Reactive oxygen species (ROS) ↑ ROS (dose-, metal-, context-dependent) ↓ ROS Conditional Driver Biphasic redox modulation Quercetin exhibits pro-oxidant behavior in cancer cells while protecting normal cells
2 Mitochondrial integrity / intrinsic apoptosis ↓ ΔΨm; ↑ caspase activation ↔ preserved Driver Execution of intrinsic apoptosis Mitochondrial dysfunction is a central apoptosis route in cancer cells
3 PI3K → AKT → mTOR axis ↓ AKT / ↓ mTOR ↔ adaptive suppression Driver Growth and survival inhibition AKT/mTOR suppression is a consistently reported upstream effect in cancer models
4 NF-κB signaling ↓ NF-κB activation ↓ inflammatory NF-κB tone Secondary Reduced survival and inflammatory transcription NF-κB inhibition contributes to chemosensitization and apoptosis susceptibility
5 MAPK signaling (JNK / p38) ↑ JNK / ↑ p38 ↔ minimal Secondary Stress-mediated apoptosis signaling MAPK activation supports apoptosis downstream of redox stress
6 Cell cycle regulation ↑ G1/S or G2/M arrest ↔ largely spared Phenotypic Cytostatic growth control Cell-cycle arrest reflects disruption of growth signaling
7 HIF-1α hypoxia signaling ↓ HIF-1α ↔ minimal Secondary Reduced hypoxia tolerance Quercetin interferes with hypoxia-driven transcriptional programs
8 NRF2 antioxidant response ↑ NRF2 (adaptive, context-dependent) ↑ NRF2 (protective) Adaptive Stress compensation NRF2 induction reflects redox buffering rather than primary cytotoxicity


Scientific Papers found: Click to Expand⟱
380- AgNPs,  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

6- Ba,  Api,  QC,    Common Botanical Compounds Inhibit the Hedgehog Signaling Pathway in Prostate Cancer
- in-vitro, Pca, PC3
HH↓, Common Botanical Compounds Inhibit the Hedgehog Signaling Pathway in Prostate Cancer
Gli1↓, three compounds, apigenin, baicalein, and quercetin, decreased Gli1 mRNA concentration but not Gli reporter activity

3633- BBR,  LT,  Cro,  QC,    Naturally Occurring Acetylcholinesterase Inhibitors and Their Potential Use for Alzheimer's Disease Therapy
- Review, AD, NA
*AChE↓, Alzheimer's disease (AD) is a main cause of dementia, accounting for up to 75% of all dementia cases. Pathophysiological processes described for AD progression involve neurons and synapses degeneration, mainly characterized by cholinergic impairment.
*AChE↓, Fig1: Berberine(1uM), Luteolin(80uM), Crocetin(100uM), Quercetin(120uM)

5643- BCA,  GEN,  QC,  SIL,  KaempF  P-glycoprotein inhibitors of natural origin as potential tumor chemo-sensitizers: A review
- in-vitro, NA, NA
P-gp↓, large number of flavonoids on P-gp inhibition. Biochanin-A, genistein, quercetin, chalcone, silymarin, phloretin, morin, and kaempferol

5753- CA,  QC,  MEL,    Effects of Caffeic Acid and Quercetin on In Vitro Permeability, Metabolism and In Vivo Pharmacokinetics of Melatonin in Rats: Potential for Herb-Drug Interaction
- in-vivo, Colon, Caco-2
BioAv↑, These findings suggest that caffeic acid and quercetin improved oral exposure of melatonin via CYP1A inhibition pathway.
CYP1A1↓,

6027- CGA,  CUR,  EGCG,  QC,  RES  Contribution of Non-Coding RNAs to Anticancer Effects of Dietary Polyphenols: Chlorogenic Acid, Curcumin, Epigallocatechin-3-Gallate, Genistein, Quercetin and Resveratrol
- Review, Nor, NA
*ROS↓, polyphenols have similar chemical and biological properties in that they can act as antioxidants and exert the anticancer effects via cell signaling pathways involving their reactive oxygen species (ROS)-scavenging activity.
ROS↑, These polyphenols may also act as pro-oxidants under certain conditions, especially at high concentrations.

6134- CHr,  QC,  RT,    Comparative Pharmacokinetics and Safety of a Micellar Chrysin–Quercetin–Rutin Formulation: A Randomized Crossover Trial
- Trial, Nor, NA
Dose↝, Sixteen healthy adults received a single oral dose of each formulation in randomized order separated by a 7-day washout. Chrysin (HPLC, %) 31.6% Quercetin (HPLC, %) 7.11% Rutin (HPLC, %) 7.73%
BioAv↑, The novel micellar chrysin–quercetin–rutin formulation substantially improved bioavailability and was well tolerated during 30 days of daily use
MPT↑, The micellar delivery matrix (LipoMicel®) enhances chrysin’s solubility and membrane permeability, while the combined antioxidant and anti-inflammatory activities of quercetin and rutin act synergistically to overcome pharmacokinetic barriers and amp
eff↑, In addition to chrysin as the primary active compound, the formulation incorporates excipients such as lecithin, and medium-chain triglycerides (MCT) which collectively function to stabilize micelle formation, improve dispersion, and enhance intesti
Half-Life↑, Furthermore, the non-significant trend toward a longer apparent half-life for LMC may indicate altered elimination kinetics or even partial enterohepatic recycling

6416- CUR,  QC,  FA,  RES,  EGCG  Natural products targeting mitochondria: emerging therapeutics for age-associated neurological disorders
- Review, AD, NA
*DRP1/DNM1L↓, Resveratrol was shown to regulate mitochondrial fusion/fission dynamics through increasing the expression of MFN2 and OPA1 while decreasing the expression of DRP1 and FIS1
*FIS1↓,
*MFN2↑, Resveratrol also increased OPA1 and MFN2 expression to promote mitochondrial fusion in the hippocampus of SAMP8 mice, a model of dementia
*OPA1↑,
*DRP1/DNM1L↓, curcumin can reduce mitochondrial fission by decreasing the expression of DRP1 and FIS1, and enhance fusion by increasing the expression of OPA1, MFN1 and MFN2 in the brains of SAMP8 mice
*FIS1↓,
*OPA1↑,
*MFN1↑,
*MFN2↑,
*DRP1/DNM1L↓, quercetin was found to regulate mitochondrial dynamics by inhibiting the expression of DRP1 and FIS1 and at the same time increasing the expression of MFN1 and MFN2 in the rat hippocampus, thereby improving hypoxia-induced memory deficits
*FIS1↓,
*MFN1↑,
*MFN2↑,
*memory↑,
*mtDam↓, EGCG was found to protect mitochondrial function by down-regulating the expression of DRP1 and FIS1 in the brain
*DRP1/DNM1L↓,
*FIS1↓,

6682- DCA,  QC,    Dichloroacetate and Quercetin Prevent Cell Proliferation, Induce Cell Death and Slow Tumor Growth in a Mouse Model of HPV-Positive Head and Neck Cancer
- in-vivo, HNSCC, MEER
PDK1↓, Dichloroacetate (DCA) is an inhibitor of pyruvate dehydrogenase kinase that decreases lactate production.
lactateProd↓,
GlucoseCon↓, Quercetin is a flavonoid compound found in fruits and vegetables that inhibits glucose uptake and lactate export.
tumCV↓, Both DCA and quercetin inhibited colony formation and reduced cell viability, which were associated with mTOR inhibition and increased apoptosis through enhanced ROS production.
mTOR↓,
Apoptosis↑,
ROS↑,
TumCG↓, DCA and quercetin reduced tumor growth and enhanced survival in immune-competent mice, correlating with decreased proliferation as well as decreased acidification of the tumor microenvironment and reduction of Foxp (+) Treg lymphocytes.
pH↑,
cl‑PARP↑, increased levels of cleaved PARP (Figure 2C) in the combination treatment as well as increased caspase 3 cleavage
Casp3↑,
DNAdam↑, DCA and Quercetin Increase DNA Damage through Enhanced ROS Production
p‑γH2AX↑, increased ROS production was correlated with increased phosphorylated H2AX, which is an indicator of ROS-induced DNA damage
eff↓, NAC can partially prevent the DCA/quercetin increased ROS production and phosphorylation of H2AX, as well as the induction of cleaved PARP.
OS↑, In addition to just prolonging survival, DCA, quercetin, and more so their combination, increased the number of animals who went on to be tumor-free.

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↑, Genistein and quercetin, as individual phytochemicals, increased NQO1 expression by ~3.78- and ~6.42-fold, respectively,
P53↑, Taken together, these results support the existence of synergy between EGCG, genistein and quercetin in the control of AR, p53 and NQO1 expression
NQO2↑,
chemoPv↑, synergy between bioactive dietary agents, thus broadening the chemopreventive index
TumCP↓, Analyzing the results from colony formation and cell proliferation together, the relative potency and efficacy of the three phytochemicals was ranked as EGCG>quercetin>genistein.
AR↓, EGCG or quercetin (2.5 μM) separately, inhibited AR expression by 67% and 47%, respectively compared to the control,

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↓, fact that EGCG primarily inhibited COMT activity, whereas quercetin reduced the amount of COMT protein.
TumCP↑, Quercetin and EGCG in combination synergistically inhibited cell proliferation, caused cell cycle arrest, and induced apoptosis in PC-3 cells.
TumCCA↑,
Apoptosis↑,

26- EGCG,  QC,  docx,    Green tea and quercetin sensitize PC-3 xenograft prostate tumors to docetaxel chemotherapy
- vitro+vivo, Pca, PC3
BAD↓,
cl‑PARP↑,
Casp7↑,
IκB↓,
Ki-67↓,
VEGF↓,
EGFR↓,
FGF↓,
TGF-β↓,
TNF-α↓,
SCF↓,
Bax:Bcl2↑,
NF-kB↓,
chemoP↑, This study provides a novel regimen to enhance the therapeutic effect of Doc in a less-toxic manner and reduce its risk of side effects in treatment of CRPC.
ChemoSen↑, GT and Q with LD Doc significantly enhanced the potency of Doc 2-fold and reduced tumor growth by 62 % compared to LD Doc in 7-weeks intervention.
TumVol↓,

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)

4687- LT,  QC,    Dietary Flavonoids Luteolin and Quercetin Suppressed Cancer Stem Cell Properties and Metastatic Potential of Isolated Prostate Cancer Cells
- in-vitro, Pca, DU145
CSCs↓, Since luteolin and quercetin were able to target CSC cells and prevent cancer cell invasiveness, may serve as potential anti-angiogenesis and anti-metastasis agents.
EMT↓, Furthermore, reversed epithelial-mesenchymal transition (EMT) to reduce MMP secretion by Lu and Qu exert inhibition of migration and invasion abilities in A431 cells
MMPs↓,
TumCMig↓,
TumCI↓,

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)

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

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

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

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

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•−

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

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↑,

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

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

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

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

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↓, quercetin suppressed EMT process, promote apoptosis and deactivated PI3K/Akt signaling pathway in PC-3 cells
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↓, MALAT1 expression was significantly downregulated in quercetin-treated PC cells at a dose- and time-dependent manne
TumCG↓, Quercetin Inhibited Tumor Growth by Targeting MALAT1 in vivo

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

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↓,

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

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.

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”.

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

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

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.

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.

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.

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

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

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)

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↓, treatment with Q+C was much more effective than either Q or C in inhibiting DNMT,
AR↑, Treatment with Q or C or Q+C resulted in a marked increase in the expression of AR protein levels in PC3 and DU145 cell lines,
MMP↓, combined treatment with Q+C was stronger than that of individual treatments (Q or C) in depolarizing the mitochondrial membrane potential

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↓, CCND1, CCND2, CCND3
cycE/CCNE↓, 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↓,
TumCCA↑, quercetin significantly inhibited the expression of specific oncogenes and genes controlling G1, S, G2, and M phases of the cell cycle.
chemoPv↑, Our results correlate with those of nutritional studies that support the roles of dietary bioflavonoids as cancer chemopreventive agents.

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.

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

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↓,

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

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


Showing Research Papers: 1 to 50 of 218
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* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 218

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

CYP1A1↓, 1,   GSH↓, 1,   GSH∅, 1,   H2O2↑, 2,   NQO1↑, 1,   OXPHOS↝, 1,   ROS↓, 1,   ROS↑, 18,   ROS⇅, 2,   TrxR↓, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

ATP↝, 1,   BCR↓, 1,   CDC16↓, 1,   MMP↓, 2,   MPT↑, 1,   OCR↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

AKT1↓, 1,   cMyc↓, 1,   ECAR↓, 1,   GlucoseCon↓, 1,   Glycolysis↓, 1,   HK2↓, 1,   lactateProd↓, 2,   PDK1↓, 1,   PI3K/Akt↓, 1,   PI3k/Akt/mTOR↓, 1,   PKM2↓, 1,  

Cell Death(tgid=5) ⓘ

Apoptosis↑, 5,   BAD↓, 1,   Bax:Bcl2↑, 1,   Casp3↑, 2,   Casp7↑, 1,   CBP↑, 1,   cFLIP↓, 1,   p‑JNK↓, 1,   MAPK↝, 1,  

Kinase & Signal Transduction(tgid=6) ⓘ

CDC7↓, 1,   HER2/EBBR2↓, 1,   TSC2↑, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

other↓, 1,   other↑, 2,   tumCV↓, 2,  

Protein Folding & ER Stress(tgid=8) ⓘ

CHOP↓, 1,   p‑eIF2α↓, 1,   p‑IRE1↓, 1,   NQO2↑, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

TumAuto↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

BRCA1↑, 1,   CUL4B↑, 1,   DNAdam↑, 1,   DNMTs↓, 1,   P53↑, 3,   cl‑PARP↑, 2,   PCNA↓, 1,   p‑γH2AX↑, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

CDK2↓, 1,   cycD1/CCND1↓, 1,   cycE/CCNE↓, 1,   cycF↓, 1,   E2Fs↓, 1,   P21↑, 1,   RB1↑, 1,   TumCCA↑, 4,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

cDC2↓, 1,   CSCs↓, 1,   EMT↓, 2,   EP300↑, 1,   ERK↝, 1,   FGF↓, 1,   Gli1↓, 1,   HH↓, 1,   mTOR↓, 2,   NF2↑, 1,   PTEN↑, 1,   SCF↓, 1,   STAT3↓, 1,   TumCG↓, 4,   Wnt/(β-catenin)↓, 1,  

Migration(tgid=13) ⓘ

CDK4/6↓, 1,   E-cadherin↑, 1,   Ki-67↓, 2,   MALAT1↓, 1,   MMP2↓, 1,   MMP9:TIMP1↓, 1,   MMPs↓, 2,   MSH2↑, 1,   N-cadherin↓, 1,   TGF-β↓, 1,   TSC1↑, 1,   TumCI↓, 1,   TumCMig↓, 1,   TumCP↓, 1,   TumCP↑, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

EGFR↓, 1,   Hif1a↓, 1,   VEGF↓, 2,  

Barriers & Transport(tgid=15) ⓘ

GLUT1↓, 1,   P-gp↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2↓, 1,   IL10↓, 1,   IL6↓, 1,   IκB↓, 1,   NF-kB↓, 1,   TNF-α↓, 2,  

Cellular Microenvironment(tgid=17) ⓘ

pH↑, 1,  

Hormonal & Nuclear Receptors(tgid=20) ⓘ

AR↓, 1,   AR↑, 1,   COMT↓, 1,   CYP19↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↑, 2,   BioEnh↑, 1,   ChemoSen↑, 2,   Dose↝, 1,   eff↓, 2,   eff↑, 2,   Half-Life↑, 1,   RadioS↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

AR↓, 1,   AR↑, 1,   BRCA1↑, 1,   EGFR↓, 1,   HER2/EBBR2↓, 1,   IL6↓, 1,   Ki-67↓, 2,  

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 2,   AntiTum↑, 1,   chemoP↑, 1,   chemoPv↑, 2,   OS↑, 1,   Risk↓, 1,   TGFβR1↑, 1,   TumVol↓, 2,  
Total Targets: 132

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 3,   Catalase↑, 1,   GSH↑, 1,   GSH⇅, 1,   lipid-P↓, 2,   MDA↓, 3,   MFN1↑, 2,   MFN2↑, 3,   OPA1↑, 2,   ROS↓, 4,   ROS↑, 1,   ROS⇅, 1,   SOD↑, 1,   TAC∅, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

ATP↑, 1,   DRP1/DNM1L↓, 4,   FIS1↓, 4,   MMP↑, 1,   mtDam↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

AMP↓, 1,   AMPK↑, 1,   NADPH↓, 2,  

Cell Death(tgid=5) ⓘ

Akt↑, 1,   GRP58↓, 1,   iNOS↓, 2,   MAPK↑, 1,   p38↑, 1,  

Protein Folding & ER Stress(tgid=8) ⓘ

ER Stress↓, 1,   UPR↓, 1,   XBP-1↓, 1,  

DNA Damage & Repair(tgid=10) ⓘ

P53↝, 1,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

PI3K↑, 1,  

Migration(tgid=13) ⓘ

AP-1↓, 1,  

Barriers & Transport(tgid=15) ⓘ

BBB↝, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

Inflam↓, 2,   NF-kB↓, 3,  

Synaptic & Neurotransmission(tgid=18) ⓘ

AChE↓, 3,   p‑tau↓, 1,  

Protein Aggregation(tgid=19) ⓘ

Aβ↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 1,   BioAv↑, 1,   BioEnh↑, 1,   Dose↑, 1,   eff↝, 1,  

Functional Outcomes(tgid=23) ⓘ

cognitive↑, 1,   memory↑, 3,   neuroP↑, 2,   radioP↑, 1,   Weight↓, 1,  
Total Targets: 49

Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include : 
  -low or high Dose
  -format for product, such as nano of lipid formations
  -different cell line effects
  -synergies with other products 
  -if effect was for normal or cancerous cells

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:140  Target#:%  State#:%  Dir#:%
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