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.
EMIQ bioavialability is about 3X that of Quercetin (Example Natural Factors brand)
Isoquercitrin is high bioaviability and efficiacy but at this time does not seem available as supplement.

-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↓, 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">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

7815-

Api,

Lut,

NarG,

QC,

MOR

The role of natural flavonoids on neuroinflammation as a therapeutic target for Alzheimer’s disease: a narrative review

Review,

AD,

*Inflam?, 13 natural flavonoids (apigenin, luteolin, naringenin, quercetin, morin, kaempferol, fisetin, isoquercitrin, astragalin, rutin, icariin, mangiferin, and anthocyanin) derived from plants or medicinal herbs on neuroinflammation in Alzheimer’s diseas

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,

*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,

P-gp/ABCB1↓, 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

Rats

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,

*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,

 novel micellar chrysin formulation co-encapsulated with quercetin and rutin (LMC) compared with a non-micellar chrysin formulation (NMC) and unformulated chrysin (UFC).

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,

*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

mouse

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

 0.1, 1, 5, 10, 50 uM

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

 5, 10, 20 uM

in-vitro,

Pca,

LNCaP

 5, 10, 20 uM

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,

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,

in-vivo,

Nor,

rat

*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)

7044-

GA,

QC,

Inhibitory effects of gallic acid and quercetin on UDP-glucose dehydrogenase activity

in-vitro,

BC,

MCF7

UGDH↓, UGDH revealed that gallic acid was a non-competitive inhibitor with respect to UDP-glucose and NAD+. I
UGDH↓, In contrast, quercetin showed a competitive inhibition and a mixed-type inhibition with respect to UDP-glucose and NAD+, respectively.
TumCP↓, gallic acid and quercetin are effective inhibitors of UGDH that exert strong antiproliferative activity in breast cancer cells.
Dose↑, The concentrations of gallic acid and quercetin needed to produce effects on UGDH are at least 10-fold higher than can be predicted to be reached under in vivo dietary conditions
*BioAv↓, oral bioavailability of polyphenols including gallic acid and quercetin is very low, producing plasma concentrations most likely only 1/10th to 1/100th of those necessary to produce an effect
eff?, However, it is still not understood if the polyphenols have to be in the free form to exert their activity, or the conjugated polyphenols can exert similar activity, as it has been reported for quercetin

7849-

ISQ,

QC,

Isoquercitrin provides better bioavailability than quercetin: comparison of quercetin metabolites in body tissue and brain sections after six days administration of isoquercitrin and quercetin

in-vivo,

Nor,

In the present study, over a period of 8 days 12 mg/kg/d quercetin aglycone and 18 mg/kg/d isoquercitrin were orally given to rats, respectively

*Dose↝, In the present study, over a period of 8 days 12 mg/kg/d quercetin aglycone and 18 mg/kg/d isoquercitrin were orally given to rats, respectively
*BioAv↑, Compared to the quercetin gavage the isoquercitrin gavage consistently produced higher levels of QM in tissues (double to five-fold) as well as in plasma (double to three-fold). I

7835-

ISQ,

QC,

Synergistic Protection by Isoquercitrin and Quercetin against Glutamate-Induced Oxidative Cell Death in HT22 Cells via Activating Nrf2 and HO-1 Signaling Pathway: Neuroprotective Principles and Mechanisms of Dendropanax morbifera Leaves

in-vitro,

AD,

HT22

*Apoptosis↓, Isoquercitrin and quercetin significantly inhibited Glu-induced oxidative cell death by restoring intracellular reactive oxygen species (ROS) levels and mitochondrial superoxide generation, Ca2+ dysregulation, mitochondrial dysfunction,
*ROS↓,
*SOD2↑,
*Ca+2↓, isoquercitrin and quercetin significantly restored Glu-induced ROS generation and Ca2+ increase in a concentration-dependent manner
*mtDam↓,
*NRF2↑, These two compounds significantly increased the expression levels of nuclear factor erythroid-2-related factor 2 (Nrf2) and heme oxygenase 1 (HO-1) in the presence or absence of Glu treatment.
*HO-1↑,
*other↑, These findings suggest that isoquercitrin and quercetin are the active principles representing the protective effects of DMLE, and these effects were mediated by the Nrf2/HO-1 pathway.
*AIF↓, Glu significantly increased nuclear levels of AIF, whereas isoquercitrin or quercetin reversed Glu-induced nuclear translocation of AIF.
*LC3‑Ⅱ/LC3‑Ⅰ↓, decreased the LC3AB-II/-I ratio to a level lower than Glu alone.
*eff↑, Combination of Isoquercitrin and Quercetin Synergistically Inhibited Glu-Induced Cell Death

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

50, 75, and 100 umol/L

<1uM

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,

30 mg/kg dissolved in Tween 80

mice

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/PTGS2↓,
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,

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,

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,

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,

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,

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,

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,

mice

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,

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,

investigated in aerated and incubated emulsions

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,

50 mg/kg

mice

*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

 50 uM; 75mg/kg/every other day

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,

<10uM

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,

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,

Rats

*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,

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,

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,

50uM

protected mouse thymocytes from glucose oxidase (GO)-mediated apoptosis

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,

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,

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,

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,

ROS↑, in the presence of the transition metal

889-

QC,

The multifaceted role of quercetin derived from its mitochondrial mechanism

vitro+vivo,

Var,

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,

*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

 0-50 uM

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,

Review,

Stroke,

*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.

Showing Research Papers: 1 to 50 of 223
Page 1 of 5 SREBP&page=2&exSp=open">Next

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 223

Pathway results for Effect on Cancer / Diseased Cells:

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 1, Catalase↑, 1, GSH↑, 1, GSH⇅, 1, HO-1↑, 1, lipid-P↓, 1, MDA↓, 3, MFN1↑, 2, MFN2↑, 3, NRF2↑, 1, OPA1↑, 2, ROS↓, 4, ROS↑, 1, ROS⇅, 1, SOD↑, 1, SOD2↑, 1, TAC∅, 1,

Mitochondria & Bioenergetics(tgid=3) ⓘ

AIF↓, 1, DRP1/DNM1L↓, 4, FIS1↓, 4, mtDam↓, 2,

Core Metabolism/Glycolysis(tgid=4) ⓘ

AMP↓, 1, NADPH↓, 1,

Cell Death(tgid=5) ⓘ

Akt↑, 1, Apoptosis↓, 1, iNOS↓, 1, MAPK↑, 1, p38↑, 1,

Transcription & Epigenetics(tgid=7) ⓘ

other↑, 1,

Autophagy & Lysosomes(tgid=9) ⓘ

LC3‑Ⅱ/LC3‑Ⅰ↓, 1,

DNA Damage & Repair(tgid=10) ⓘ

P53↝, 1,

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

PI3K↑, 1,

Migration(tgid=13) ⓘ

AP-1↓, 1, Ca+2↓, 1,

Immune & Inflammatory Signaling(tgid=16) ⓘ

Inflam?, 1, NF-kB↓, 2,

Synaptic & Neurotransmission(tgid=18) ⓘ

AChE↓, 2,

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 1, BioAv↑, 2, BioEnh↑, 1, Dose↑, 1, Dose↝, 1, eff↑, 1, eff↝, 1,

Functional Outcomes(tgid=23) ⓘ

memory↑, 2, neuroP↑, 1, radioP↑, 1, Weight↓, 1,
Total Targets: 48

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#:%
  wNotes=on  sortOrder:rid,rpid

Quercetin Cancer Research Results

Pathway results for Effect on Cancer / Diseased Cells:

NA, unassigned(tgid=0) ⓘ

Redox & Oxidative Stress(tgid=1) ⓘ

Mitochondria & Bioenergetics(tgid=3) ⓘ

Core Metabolism/Glycolysis(tgid=4) ⓘ

Cell Death(tgid=5) ⓘ

Kinase & Signal Transduction(tgid=6) ⓘ

Transcription & Epigenetics(tgid=7) ⓘ

Protein Folding & ER Stress(tgid=8) ⓘ

Autophagy & Lysosomes(tgid=9) ⓘ

DNA Damage & Repair(tgid=10) ⓘ

Cell Cycle & Senescence(tgid=11) ⓘ

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

Migration(tgid=13) ⓘ

Angiogenesis & Vasculature(tgid=14) ⓘ

Barriers & Transport(tgid=15) ⓘ

Immune & Inflammatory Signaling(tgid=16) ⓘ

Cellular Microenvironment(tgid=17) ⓘ

Hormonal & Nuclear Receptors(tgid=20) ⓘ

Drug Metabolism & Resistance(tgid=21) ⓘ

Clinical Biomarkers(tgid=22) ⓘ

Functional Outcomes(tgid=23) ⓘ

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress(tgid=1) ⓘ

Mitochondria & Bioenergetics(tgid=3) ⓘ

Core Metabolism/Glycolysis(tgid=4) ⓘ

Cell Death(tgid=5) ⓘ

Transcription & Epigenetics(tgid=7) ⓘ

Autophagy & Lysosomes(tgid=9) ⓘ

DNA Damage & Repair(tgid=10) ⓘ

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

Migration(tgid=13) ⓘ

Immune & Inflammatory Signaling(tgid=16) ⓘ

Synaptic & Neurotransmission(tgid=18) ⓘ

Drug Metabolism & Resistance(tgid=21) ⓘ

Functional Outcomes(tgid=23) ⓘ

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