Quercetin / tumCV 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 (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


tumCV, Cell Viability: Click to Expand ⟱
Source:
Type:
Cell Viability
Scientific Papers found: Click to Expand⟱
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↓, lactateProd↓, GlucoseCon↓, tumCV↓, mTOR↓, Apoptosis↑, ROS↑, TumCG↓, pH↑, cl‑PARP↑, Casp3↑, DNAdam↑, p‑γH2AX↑, eff↓, OS↑,
910- QC,    The Anti-Cancer Effect of Quercetin: Molecular Implications in Cancer Metabolism
tumCV↓, Apoptosis↑, PI3k/Akt/mTOR↓, Wnt/(β-catenin)↓, MAPK↝, ERK↝, TumCCA↑, H2O2↑, ROS↑, TumAuto↑, MMPs↓, P53↑, Casp3↑, Hif1a↓, cFLIP↓, IL6↓, IL10↓, lactateProd↓, Glycolysis↓, PKM2↓, GLUT1↓, COX2/PTGS2↓, VEGF↓, OCR↓, ECAR↓, STAT3↓, MMP2↓, MMP9:TIMP1↓, mTOR↓,
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↑, DNAdam↑, Chk2↑, CycB/CCNB1↓, CDK1↓, tumCV↓, p‑RB1↓, P21↑,
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↓, MMPs↓, MMP2↓, MMP7↓, STAT3↓, TumCI↓, TumMeta↓, tumCV↓,
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, MCF7 - in-vitro, BC, MDA-MB-231
EGFR↓, PI3k/Akt/mTOR↓, GSK‐3β↓, TumCP↓, Apoptosis↑, tumCV↓, mTOR↓, PTEN↑,
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/CCND1↓, survivin↓, Wnt/(β-catenin)↓, tumCV↓, TumCCA↑, Apoptosis↑,
90- QC,  HYP,    Combination of quercetin and hyperoside inhibits prostate cancer cell growth and metastasis via regulation of microRNA‑21
- in-vitro, Pca, PC3
ROS↑, cl‑Casp3↑, cl‑PARP↑, miR-21↓, PDCD4↑, TAC↑, tumCV↓, TumCI↓,
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↓, TCF↓, eff↑, CSCs↓, TumCG↓, tumCV↓,
3339- QC,    Quercetin suppresses ROS production and migration by specifically targeting Rac1 activation in gliomas
- in-vitro, GBM, C6 - in-vitro, GBM, IMR32
BBB↑, tumCV↓, TumCMig↓, Rac1↓, p66Shc↓, ROS↓,
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↓, selectivity↑, TumCCA↑, TumCMig↓, TumCI↓, Apoptosis↑, TumMeta↓, Bcl-2↓, BAX↑, TIMP1↑, MMP2↓, MMP9↓, *Inflam↓, *neuroP↑, *cardioP↑, p38↓, MAPK↓, Twist↓, P21↓, cycD1/CCND1↓, Casp3↑, Casp9↑, p‑Akt↓, p‑ERK↓, CD44↓, CD24↓, ChemoSen↑, MMP↓, Cyt‑c↑, AIF↑, ROS↑, Ca+2↑, Hif1a↓, VEGF↓,
3343- QC,    Quercetin, a Flavonoid with Great Pharmacological Capacity
- Review, Var, NA - Review, AD, NA - Review, Arthritis, NA
*antiOx↑, *ROS↓, *angioG↓, *Inflam↓, *BioAv↓, *Half-Life↑, *GSH↑, *SOD↑, *Catalase↑, *Nrf1↑, *BP↓, *cardioP↑, *IL10↓, *TNF-α↓, *Aβ↓, *GSK‐3β↓, *tau↓, *neuroP↑, *Pain↓, *COX2/PTGS2↓, *NRF2↑, *HO-1↑, *IL1β↓, *IL17↓, *MCP1/CCL2↓, PKCδ↓, ERK↓, BAX↓, cMyc↓, KRAS↓, ROS↓, selectivity↑, tumCV↓, Apoptosis↑, TumCCA↑, eff↑, P-gp/ABCB1↓, eff↑, eff↑, eff↑, eff↑, CycB/CCNB1↓, CDK1↓, CDK4↓, CDK2↓, TOP2↓, Cyt‑c↑, cl‑PARP↑, MMP↓, HSP70/HSPA5↓, HSP90↓, MDM2↓, RAS↓, eff↑,
3379- QC,    The Effect of Quercetin Nanosuspension on Prostate Cancer Cell Line LNCaP via Hedgehog Signaling Pathway
- in-vitro, Pca, LNCaP
tumCV↓, HH↓,
3376- QC,    Inhibiting CDK6 Activity by Quercetin Is an Attractive Strategy for Cancer Therapy
- in-vitro, BC, MCF7 - in-vitro, Lung, A549
CDK6↓, tumCV↓, Apoptosis↑, ROS↓, eff↑,
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↓, α-SMA↑, TumCP↓, tumCV↓, TumVol↓, TumCI↓, TumMeta↓, TumCMig↓, ROS↑, Apoptosis↑, BioAv↓, *neuroP↑, *antiOx↑, *Inflam↓, *Aβ↓, *cardioP↑, MMP↓, Cyt‑c↑, MMP2↓, MMP9↓, EMT↓, MMPs↓, Twist↓, Slug↓, Ca+2↑, AIF↑, Endon↑, P-gp/ABCB1↓, LDH↑, HK2↓, PKA↓, Glycolysis↓, GlucoseCon↓, lactateProd↓, GRP78/BiP↑, Casp12↑, CHOP/DDIT3↑,
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↑, cycD1/CCND1↓, Casp3↑, GRP78/BiP↑, CHOP/DDIT3↑, tumCV↓, IRE1↑, p‑PERK↑, c-ATF6↑, ER Stress↑,
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↑, PARP↑, survivin↓, miR-27a-3p↓, Sp1/3/4↓, ZBTB10↑, ROS⇅, TAC↑, tumCV↓,

Showing Research Papers: 1 to 16 of 16

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 16

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

H2O2↑, 1,   p66Shc↓, 1,   ROS↓, 3,   ROS↑, 5,   ROS⇅, 1,   TAC↑, 2,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

AIF↑, 2,   MMP↓, 3,   OCR↓, 1,   XIAP↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

cMyc↓, 1,   ECAR↓, 1,   GlucoseCon↓, 2,   Glycolysis↓, 2,   HK2↓, 1,   lactateProd↓, 3,   LDH↑, 1,   PDK1↓, 1,   PI3k/Akt/mTOR↓, 2,   PKM2↓, 1,  

Cell Death(tgid=5) ⓘ

p‑Akt↓, 1,   Apoptosis↑, 9,   BAX↓, 1,   BAX↑, 1,   Bcl-2↓, 2,   Casp12↑, 1,   Casp3↑, 6,   cl‑Casp3↑, 1,   Casp7↑, 1,   Casp9↑, 1,   cFLIP↓, 1,   Chk2↑, 1,   Cyt‑c↑, 3,   Endon↑, 1,   MAPK↓, 1,   MAPK↝, 1,   MDM2↓, 1,   p38↓, 1,   PDCD4↑, 1,   survivin↓, 3,  

Kinase & Signal Transduction(tgid=6) ⓘ

Sp1/3/4↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

miR-21↓, 1,   miR-27a-3p↓, 1,   tumCV↓, 16,  

Protein Folding & ER Stress(tgid=8) ⓘ

c-ATF6↑, 1,   CHOP/DDIT3↑, 2,   ER Stress↑, 1,   GRP78/BiP↑, 2,   HSP70/HSPA5↓, 1,   HSP90↓, 1,   IRE1↑, 1,   p‑PERK↑, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

TumAuto↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

DNAdam↑, 2,   P53↑, 1,   PARP↑, 1,   cl‑PARP↑, 3,   p‑γH2AX↑, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

CDK1↓, 2,   CDK2↓, 1,   CDK4↓, 1,   CycB/CCNB1↓, 2,   cycD1/CCND1↓, 3,   P21↓, 1,   P21↑, 1,   p‑RB1↓, 1,   TumCCA↑, 5,  

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

CD24↓, 1,   CD44↓, 1,   CSCs↓, 1,   EMT↓, 3,   ERK↓, 1,   ERK↝, 1,   p‑ERK↓, 1,   GSK‐3β↓, 1,   HH↓, 1,   mTOR↓, 3,   PTEN↑, 1,   RAS↓, 1,   STAT3↓, 2,   TCF↓, 1,   TOP2↓, 1,   TumCG↓, 2,   Wnt/(β-catenin)↓, 2,  

Migration(tgid=13) ⓘ

Ca+2↑, 2,   KRAS↓, 1,   LEF1↓, 1,   MMP2↓, 4,   MMP7↓, 1,   MMP9↓, 2,   MMP9:TIMP1↓, 1,   MMPs↓, 3,   PKA↓, 1,   PKCδ↓, 1,   Rac1↓, 1,   Slug↓, 2,   Snail↓, 1,   TIMP1↑, 1,   TumCI↓, 4,   TumCMig↓, 3,   TumCP↓, 3,   TumMeta↓, 3,   Twist↓, 2,   Vim↓, 1,   α-SMA↓, 1,   α-SMA↑, 1,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

EGFR↓, 1,   Hif1a↓, 2,   VEGF↓, 2,   ZBTB10↑, 1,  

Barriers & Transport(tgid=15) ⓘ

BBB↑, 1,   GLUT1↓, 1,   P-gp/ABCB1↓, 2,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2/PTGS2↓, 1,   IL10↓, 1,   IL6↓, 1,  

Cellular Microenvironment(tgid=17) ⓘ

pH↑, 1,  

Hormonal & Nuclear Receptors(tgid=20) ⓘ

CDK6↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 1,   ChemoSen↑, 1,   eff↓, 1,   eff↑, 8,   selectivity↑, 2,  

Clinical Biomarkers(tgid=22) ⓘ

EGFR↓, 1,   IL6↓, 1,   KRAS↓, 1,   LDH↑, 1,  

Functional Outcomes(tgid=23) ⓘ

OS↑, 1,   TumVol↓, 1,  
Total Targets: 130

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 2,   Catalase↑, 1,   GSH↑, 1,   HO-1↑, 1,   Nrf1↑, 1,   NRF2↑, 1,   ROS↓, 1,   SOD↑, 1,  

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

GSK‐3β↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2/PTGS2↓, 1,   IL10↓, 1,   IL17↓, 1,   IL1β↓, 1,   Inflam↓, 3,   MCP1/CCL2↓, 1,   TNF-α↓, 1,  

Synaptic & Neurotransmission(tgid=18) ⓘ

tau↓, 1,  

Protein Aggregation(tgid=19) ⓘ

Aβ↓, 2,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 1,   Half-Life↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

BP↓, 1,  

Functional Outcomes(tgid=23) ⓘ

cardioP↑, 3,   neuroP↑, 3,   Pain↓, 1,  
Total Targets: 25

Scientific Paper Hit Count for: tumCV, Cell Viability
16 Quercetin
1 Dichloroacetate
1 Gold NanoParticles
1 Hyperoside
1 EGCG (Epigallocatechin Gallate)
1 Resveratrol
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#:897  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

 

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