Quercetin / Risk 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↓, 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


Risk, Risk: Click to Expand ⟱
Source:
Type:
Risk: by definition reduces risk of disease or cancer.
Down Target direction of risk indicates lower cancer risk.
ChemoPreventive also mean lower cancer risk. But for Chemopreventive an up arrow indicates more preventive. 
Cancer Risk Impact Score (CRIS)
CRIS scale:
–5 = very strong risk reduction
–4 = strong risk reduction
–3 = moderate risk reduction
–2 = modest risk reduction
–1 = weak / context-dependent
0 = neutral




CRIS Exposure / Compound Evidence Cancers Notes




-5 Exercise (overall)
VStrong Hum BC, CRC, Endo, PCa, Liv






-5 Aerobic + resistance VStrong Hum Broad inc + mort






-4 Aerobic exercise (mod–vig) VStrong Hum BC, CRC, Endo






-4 Resistance training (alone) Strong Hum BC, CRC






-3 High-intensity interval training Mod–Strong Hum BC, CRC






-2 NEAT / low-intensity activity Moderate Hum CRC






-5 Cruciferous vegetable pattern Strong Hum Lung, CRC, BC, PCa






-5 Sunlight exposure (physiologic) Strong Hum CRC, BC, PCa






-4 Fasting (metabolic pattern)
Strong Mech + Hum BC, CRC, PCa 






-4 Curcumin
Hum + Pre GI, BC, PCa






-4 Sulforaphane
Hum + Pre Lung, CRC, BC






-4 PEITC
Hum + Pre Lung, CRC, PCa






-4 EGCG (tea matrix)
Strong Hum GI, PCa, BC






-4 Lycopene
Strong Hum PCa






-4 Apigenin
Pre + Diet Hum BC, PCa, CRC 






-4 Luteolin
Pre + Diet Hum Lung, CRC, BC 






-4 Kaempferol
Diet Hum Ov, Panc, Lung






-4 Fisetin
Pre + Early Hum CRC, PCa, Mel






-4 Ellagic acid → Urolithin A
Hum (microbiome) CRC, PCa, BC






-3 Omega-3 (EPA/DHA)
Strong Hum CRC, BC






-3 Vitamin D3 (supp)
Obs + RCT CRC, BC






-3 Garlic (allicin)
Mod Hum GI






-3 Mushroom beta-glucans
Hum adjunct GI, BC






-3 Melatonin
Hum + Mech BC, PCa






-3 Coffee (whole)
Strong Hum Liv, Endo






-2 Quercetin
Limited Hum Lung, CRC






-2 Resveratrol
Limited Hum CRC, BC






-2 I3C / DIM
Mod Hum BC, Cerv






-2 Thymoquinone
Early Hum BC, CRC






-2 Beta-carotene (food)
Hum Lung






-1 Vitamin K2 (MK-4/7)
Limited Hum Liv, PCa






-1 Boron
Obs PCa, Lung






0 Vitamin C (oral)
Strong Hum —






0 Genistein (soy)
Strong Hum BC, PCa






0 Selenium (diet)
Mixed Hum PCa






0 Capsaicin
Mixed Gastric






+2 Vitamin E (alpha only)
Strong RCT PCa






+2 Green tea extract (high-dose)
Case reports Liv






+4 Beta-carotene (supplement)
Strong RCT Lung (smokers)






+5 Alcohol (ethanol)
Strong Hum BC, Liv, Eso







Evidence
Hum        human data
VStrong    very strong
Strong     strong
Mod        moderate
Obs        observational
Pre        preclinical
RCT        randomized controlled trial
Mech       mechanistic
Adjunct    adjunct clinical use


Scientific Papers found: Click to Expand⟱
911- QC,  SFN,    Pilot study evaluating broccoli sprouts in advanced pancreatic cancer (POUDER trial) - study protocol for a randomized controlled trial
TumCG↓, Risk↓,

Showing Research Papers: 1 to 1 of 1

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 1

Pathway results for Effect on Cancer / Diseased Cells:


Proliferation, Differentiation & Cell State ⓘ

TumCG↓, 1,  

Functional Outcomes ⓘ

Risk↓, 1,  
Total Targets: 2

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: Risk, Risk
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#:785  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

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