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↓, 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


, aggregation: Click to Expand ⟱
Source:
Type:
Beta-Amyloid (): In Alzheimer’s disease, peptides tend to misfold and aggregate into oligomers and fibrils.


Scientific Papers found: Click to Expand⟱
3336- QC,    Neuroprotective Effects of Quercetin in Alzheimer’s Disease
- Review, AD, NA
*neuroP↑, *lipid-P↓, *antiOx↑, *↓, *Inflam↓, *BBB↝, *NF-kB↓, *iNOS↓, *memory↑, *cognitive↑, *AChE↓, *MMP↑, *ROS↓, *ATP↑, *AMPK↑, *NADPH↓, *p‑tau↓,
3604- QC,    Quercetin enrich diet during the early-middle not middle-late stage of alzheimer’s disease ameliorates cognitive dysfunction
- in-vivo, AD, NA
*cognitive↑, *↓, *neuroP↑, *BACE↓, *p‑SMAD2↓, *p‑STAT3↓, *SPARC↓,
3605- QC,    Protective effect of quercetin in primary neurons against (1–42): relevance to Alzheimer's disease
- Review, AD, NA
*↓, *ROS↓, *lipid-P↓, *Apoptosis↓,
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↓, STAT↓, Inflam↓, NO↓, COX2↓, CRP↓, selectivity↑, *neuroP↑, STAT3↓, cycD1/CCND1↓, MMP2↓, STAT4↓, JAK2↓, TumCP↓, Diff↓, *eff↑, *IL6↓, *TNF-α↓, *IL1β↓, *↓,
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↓, *↓, *GSK‐3β↓, *tau↓, *neuroP↑, *Pain↓, *COX2↓, *NRF2↑, *HO-1↑, *IL1β↓, *IL17↓, *MCP1↓, PKCδ↓, ERK↓, BAX↓, cMyc↓, KRAS↓, ROS↓, selectivity↑, tumCV↓, Apoptosis↑, TumCCA↑, eff↑, P-gp↓, eff↑, eff↑, eff↑, eff↑, CycB/CCNB1↓, CDK1↓, CDK4↓, CDK2↓, TOP2↓, Cyt‑c↑, cl‑PARP↑, MMP↓, HSP70/HSPA5↓, HSP90↓, MDM2↓, RAS↓, 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↓, *↓, *cardioP↑, MMP↓, Cyt‑c↑, MMP2↓, MMP9↓, EMT↓, MMPs↓, Twist↓, Slug↓, Ca+2↑, AIF↑, Endon↑, P-gp↓, LDH↑, HK2↓, PKA↓, Glycolysis↓, GlucoseCon↓, lactateProd↓, GRP78/BiP↑, Casp12↑, CHOP↑,
6058- SeNPs,  RES,  QC,  CAR,    Engineered nanoplatforms for brain-targeted co-delivery of phytochemicals in Alzheimer's disease: Rational design, blood-brain barrier penetration, and multi-target therapeutic synergy
- Review, AD, NA
*DDS↑, *cognitive↑, *↓, *tau↓, *Inflam↓, *antiOx↑, *BioAv↑, *BioAv↑, *neuroP↑, *BioAv↑, *AChE↓,

Showing Research Papers: 1 to 7 of 7

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 7

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress

ROS↓, 1,   ROS↑, 1,  

Mitochondria & Bioenergetics

AIF↑, 1,   MMP↓, 2,  

Core Metabolism/Glycolysis

cMyc↓, 1,   GlucoseCon↓, 1,   Glycolysis↓, 1,   HK2↓, 1,   lactateProd↓, 1,   LDH↑, 1,  

Cell Death

Apoptosis↑, 2,   BAX↓, 1,   Casp12↑, 1,   Cyt‑c↑, 2,   Endon↑, 1,   MDM2↓, 1,  

Transcription & Epigenetics

tumCV↓, 2,  

Protein Folding & ER Stress

CHOP↑, 1,   GRP78/BiP↑, 1,   HSP70/HSPA5↓, 1,   HSP90↓, 1,  

DNA Damage & Repair

cl‑PARP↑, 1,  

Cell Cycle & Senescence

CDK1↓, 1,   CDK2↓, 1,   CDK4↓, 1,   CycB/CCNB1↓, 1,   cycD1/CCND1↓, 1,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State

Diff↓, 1,   EMT↓, 1,   ERK↓, 1,   RAS↓, 1,   STAT↓, 1,   STAT3↓, 1,   STAT4↓, 1,   TOP2↓, 1,  

Migration

Ca+2↑, 1,   KRAS↓, 1,   MMP2↓, 2,   MMP9↓, 1,   MMPs↓, 1,   PKA↓, 1,   PKCδ↓, 1,   Slug↓, 1,   TumCI↓, 1,   TumCMig↓, 1,   TumCP↓, 2,   TumMeta↓, 1,   Twist↓, 1,   α-SMA↓, 1,   α-SMA↑, 1,  

Angiogenesis & Vasculature

NO↓, 1,  

Barriers & Transport

P-gp↓, 2,  

Immune & Inflammatory Signaling

COX2↓, 1,   CRP↓, 1,   Inflam↓, 1,   JAK↓, 1,   JAK2↓, 1,  

Drug Metabolism & Resistance

BioAv↓, 1,   eff↑, 6,   selectivity↑, 2,  

Clinical Biomarkers

CRP↓, 1,   KRAS↓, 1,   LDH↑, 1,  

Functional Outcomes

TumVol↓, 1,  
Total Targets: 65

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress

antiOx↑, 4,   Catalase↑, 1,   GSH↑, 1,   HO-1↑, 1,   lipid-P↓, 2,   Nrf1↑, 1,   NRF2↑, 1,   ROS↓, 3,   SOD↑, 1,  

Mitochondria & Bioenergetics

ATP↑, 1,   MMP↑, 1,  

Core Metabolism/Glycolysis

AMPK↑, 1,   NADPH↓, 1,  

Cell Death

Apoptosis↓, 1,   iNOS↓, 1,  

Proliferation, Differentiation & Cell State

GSK‐3β↓, 1,   p‑STAT3↓, 1,  

Migration

p‑SMAD2↓, 1,   SPARC↓, 1,  

Angiogenesis & Vasculature

angioG↓, 1,  

Barriers & Transport

BBB↝, 1,  

Immune & Inflammatory Signaling

COX2↓, 1,   IL10↓, 1,   IL17↓, 1,   IL1β↓, 2,   IL6↓, 1,   Inflam↓, 4,   MCP1↓, 1,   NF-kB↓, 1,   TNF-α↓, 2,  

Synaptic & Neurotransmission

AChE↓, 2,   tau↓, 2,   p‑tau↓, 1,  

Protein Aggregation

↓, 7,   BACE↓, 1,  

Drug Metabolism & Resistance

BioAv↓, 1,   BioAv↑, 3,   DDS↑, 1,   eff↑, 1,   Half-Life↑, 1,  

Clinical Biomarkers

BP↓, 1,   IL6↓, 1,  

Functional Outcomes

cardioP↑, 2,   cognitive↑, 3,   memory↑, 1,   neuroP↑, 6,   Pain↓, 1,  
Total Targets: 47

Scientific Paper Hit Count for: , aggregation
7 Quercetin
1 Selenium NanoParticles
1 Resveratrol
1 Carvacrol
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#:1333  State#:%  Dir#:%
wNotes=0 sortOrder:rid,rpid

 

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