Quercetin / cMyc 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


cMyc, cellular-MYC oncogene: Click to Expand ⟱
Source:
Type: oncogene
The MYC proto-oncogenes are among the most commonly activated proteins in human cancer. The oncogene c-myc, which is frequently over-expressed in cancer cells, is involved in the transactivation of most of the glycolytic enzymes including lactate dehydrogenase A (LDHA) and the glucose transporter GLUT1 [51,52]. Thus, c-myc activation is a likely candidate to promote the enhanced glucose uptake and lactate release in the proliferating cancer cell. The c-Myc oncogene is a ‘master regulator’ of both cellular growth and metabolism in transformed cells.
-C-myc is a common oncogene that enhances aerobic glycolysis in the cancer cells by transcriptionally activating GLUT1, HK2, PKM2 and LDH-A

Inhibitors (downregulate):
Curcumin
Resveratrol: downregulate c-Myc expression.
Epigallocatechin Gallate (EGCG)
Quercetin
Berberine: decrease c-Myc expression and repress its transcriptional activity.


Scientific Papers found: Click to Expand⟱
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↓, cycE/CCNE↓, CDK2↓, CDK4/6↓, E2Fs↓, PCNA↓, cDC2↓, PTEN↑, MSH2↑, P21↑, EP300↑, BRCA1↑, NF2↑, TSC1↑, TGFβR1↑, P53↑, RB1↑, AKT1↓, cMyc↓, CDC7↓, cycF↓, CDC16↓, CUL4B↑, CBP↑, TSC2↑, HER2/EBBR2↓, BCR↓, TumCCA↑, chemoPv↑,
923- QC,    Quercetin as an innovative therapeutic tool for cancer chemoprevention: Molecular mechanisms and implications in human health
- Review, Var, NA
ROS↑, GSH↓, Ca+2↝, MMP↓, Casp3↑, Casp8↑, Casp9↑, other↓, *ROS↓, *NRF2↑, HO-1↑, TumCCA↑, Inflam↓, STAT3↓, DR5↑, P450↓, MMPs↓, IFN-γ↓, IL6↓, COX2↓, IL8↓, iNOS↓, TNF-α↓, cl‑PARP↑, Apoptosis↑, P53↑, Sp1/3/4↓, survivin↓, TRAILR↑, Casp10↑, DFF45↑, TNFR 1↑, Fas↑, NF-kB↓, IKKα↓, cycD1/CCND1↓, Bcl-2↓, BAX↑, PI3K↓, Akt↓, E-cadherin↓, Vim↓, β-catenin/ZEB1↓, cMyc↓, EMT↓, MMP2↓, NOTCH1↓, MMP7↓, angioG↓, TSP-1↑, CSCs↓, XIAP↓, Snail↓, Slug↓, LEF1↓, P-gp↓, EGFR↓, GSK‐3β↓, mTOR↓, RAGE↓, HSP27↓, VEGF↓, TGF-β↓, COL1↓, COL3A1↓,
916- QC,    Quercetin and cancer: new insights into its therapeutic effects on ovarian cancer cells
- Review, Ovarian, NA
COX2↓, CRP↓, ER Stress↑, Apoptosis↑, GRP78/BiP↑, CHOP↑, p‑STAT3↓, PI3K↓, Akt↓, mTOR↓, cMyc↓, cycD1/CCND1↓, cFLIP↓, IL6↓, IL10↓,
53- QC,    Quercetin regulates β-catenin signaling and reduces the migration of triple negative breast cancer
- in-vitro, BC, MDA-MB-231 - NA, NA, MDA-MB-468
E-cadherin↑, Vim↓, cycD1/CCND1↓, cMyc↓, EMT↓, TumCG↓, TumCMig↓, β-catenin/ZEB1↓, ChemoSen↑,
66- QC,    Emerging impact of quercetin in the treatment of prostate cancer
- Review, Pca, NA
CycB/CCNB1↓, CDK1↓, EMT↓, PI3K↓, MAPK↓, Wnt/(β-catenin)↓, PSA↓, VEGF↓, PARP↑, Casp3↑, Casp9↑, DR5↑, ROS⇅, Shh↓, P53↑, P21↑, EGFR↓, TumCCA↑, ROS↑, miR-21↓, TumCP↓, selectivity↑, PDGF↓, EGF↓, TNF-α↓, VEGFR2↓, mTOR↓, cMyc↓, MMPs↓, GRP78/BiP↑, CHOP↑,
4686- QC,    Quercetin suppresses endometrial cancer stem cells via ERα-mediated inhibition of STAT3 signaling
- in-vitro, EC, EMN8 - in-vitro, EC, EMN21
CSCs↓, ALDH1A1↓, cMyc↓, Nanog↓, OCT4↓, STAT3↓, JAK2↓, STAT3↓, eff↑,
3354- QC,    Quercetin: Its Main Pharmacological Activity and Potential Application in Clinical Medicine
- Review, Var, NA
*ROS↓, *IronCh↓, *lipid-P↓, *GSH↑, *NRF2↑, TumCCA↑, ER Stress↑, P53↑, CDK2↓, cycA1/CCNA1↓, CycB/CCNB1↓, cycE/CCNE↓, cycD1/CCND1↓, PCNA↓, P21↑, p27↑, PI3K↓, Akt↓, mTOR↓, STAT3↓, cFLIP↓, cMyc↓, survivin↓, DR5↓, *Inflam↓, *IL6↓, *IL8↓, COX2↓, 5LO↓, *cardioP↑, *FASN↓, *AntiAg↑, *MDA↓,
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↓, *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↑,
3369- QC,    Pharmacological basis and new insights of quercetin action in respect to its anti-cancer effects
- Review, Pca, NA
FAK↓, TumCCA↑, p‑pRB↓, CDK2↑, CycB/CCNB1↓, CDK1↓, EMT↓, PI3K↓, MAPK↓, Wnt↓, ROS↑, miR-21↑, Akt↓, NF-kB↓, FasL↑, Bak↑, BAX↑, Bcl-2↓, Casp3↓, Casp9↑, P53↑, p38↑, MAPK↑, Cyt‑c↑, PARP↓, CHOP↑, ROS↓, LDH↑, GRP78/BiP↑, ERK↑, MDA↓, SOD↑, GSH↑, NRF2↑, VEGF↓, PDGF↓, EGF↓, FGF↓, TNF-α↓, TGF-β↓, VEGFR2↓, EGFR↓, FGFR1↓, mTOR↓, cMyc↓, MMPs↓, LC3B-II↑, Beclin-1↑, IL1β↓, CRP↓, IL10↓, COX2↓, IL6↓, TLR4↓, Shh↓, HER2/EBBR2↓, NOTCH↓, DR5↑, HSP70/HSPA5↓, CSCs↓, angioG↓, MMP2↓, MMP9↓, IGFBP3↑, uPA↓, uPAR↓, RAS↓, Raf↓, TSP-1↑,
3368- QC,    The potential anti-cancer effects of quercetin on blood, prostate and lung cancers: An update
- Review, Var, NA
*Inflam↓, *antiOx↑, *AntiCan↑, Casp3↓, p‑Akt↓, p‑mTOR↓, p‑ERK↓, β-catenin/ZEB1↓, Hif1a↓, AntiAg↓, VEGFR2↓, EMT↓, EGFR↓, MMP2↓, MMP↓, TumMeta↓, MMPs↓, Akt↓, Snail↓, N-cadherin↓, Vim↓, E-cadherin↑, STAT3↓, TGF-β↓, ROS↓, P53↑, BAX↑, PKCδ↓, PI3K↓, COX2↓, cFLIP↓, cycD1/CCND1↓, cMyc↓, IL6↓, IL10↓, Cyt‑c↑, TumCCA↑, DNMTs↓, HDAC↓, ac‑H3↑, ac‑H4↑, Diablo↑, Casp3↑, Casp9↑, PARP1↑, eff↑, PTEN↑, VEGF↓, NO↓, iNOS↓, ChemoSen↑, eff↑, eff↑, eff↑, uPA↓, CXCR4↓, CXCL12↓, CLDN2↓, CDK6↓, MMP9↓, TSP-1↑, Ki-67↓, PCNA↓, ROS↑, ER Stress↑,

Showing Research Papers: 1 to 10 of 10

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 10

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress

GSH↓, 1,   GSH↑, 1,   HO-1↑, 1,   MDA↓, 1,   NRF2↑, 1,   ROS↓, 3,   ROS↑, 4,   ROS⇅, 1,   SOD↑, 1,  

Mitochondria & Bioenergetics

BCR↓, 1,   CDC16↓, 1,   EGF↓, 2,   FGFR1↓, 1,   MMP↓, 3,   Raf↓, 1,   XIAP↓, 1,  

Core Metabolism/Glycolysis

AKT1↓, 1,   cMyc↓, 10,   LDH↑, 1,  

Cell Death

Akt↓, 5,   p‑Akt↓, 1,   Apoptosis↑, 3,   Bak↑, 1,   BAX↓, 1,   BAX↑, 3,   Bcl-2↓, 2,   Casp10↑, 1,   Casp3↓, 2,   Casp3↑, 3,   Casp8↑, 1,   Casp9↑, 4,   CBP↑, 1,   cFLIP↓, 3,   Cyt‑c↑, 3,   Diablo↑, 1,   DR5↓, 1,   DR5↑, 3,   Fas↑, 1,   FasL↑, 1,   iNOS↓, 2,   MAPK↓, 2,   MAPK↑, 1,   MDM2↓, 1,   p27↑, 1,   p38↑, 1,   survivin↓, 2,   TNFR 1↑, 1,   TRAILR↑, 1,  

Kinase & Signal Transduction

CDC7↓, 1,   HER2/EBBR2↓, 2,   Sp1/3/4↓, 1,   TSC2↑, 1,  

Transcription & Epigenetics

ac‑H3↑, 1,   ac‑H4↑, 1,   miR-21↓, 1,   miR-21↑, 1,   other↓, 1,   p‑pRB↓, 1,   tumCV↓, 1,  

Protein Folding & ER Stress

CHOP↑, 3,   ER Stress↑, 3,   GRP78/BiP↑, 3,   HSP27↓, 1,   HSP70/HSPA5↓, 2,   HSP90↓, 1,  

Autophagy & Lysosomes

Beclin-1↑, 1,   LC3B-II↑, 1,  

DNA Damage & Repair

BRCA1↑, 1,   CUL4B↑, 1,   DFF45↑, 1,   DNMTs↓, 1,   P53↑, 6,   PARP↓, 1,   PARP↑, 1,   cl‑PARP↑, 2,   PARP1↑, 1,   PCNA↓, 3,  

Cell Cycle & Senescence

CDK1↓, 3,   CDK2↓, 3,   CDK2↑, 1,   CDK4↓, 1,   cycA1/CCNA1↓, 1,   CycB/CCNB1↓, 4,   cycD1/CCND1↓, 6,   cycE/CCNE↓, 2,   cycF↓, 1,   E2Fs↓, 1,   P21↑, 3,   RB1↑, 1,   TumCCA↑, 7,  

Proliferation, Differentiation & Cell State

ALDH1A1↓, 1,   cDC2↓, 1,   CSCs↓, 3,   EMT↓, 5,   EP300↑, 1,   ERK↓, 1,   ERK↑, 1,   p‑ERK↓, 1,   FGF↓, 1,   GSK‐3β↓, 1,   HDAC↓, 1,   IGFBP3↑, 1,   mTOR↓, 5,   p‑mTOR↓, 1,   Nanog↓, 1,   NF2↑, 1,   NOTCH↓, 1,   NOTCH1↓, 1,   OCT4↓, 1,   PI3K↓, 6,   PTEN↑, 2,   RAS↓, 2,   Shh↓, 2,   STAT3↓, 5,   p‑STAT3↓, 1,   TOP2↓, 1,   TumCG↓, 1,   Wnt↓, 1,   Wnt/(β-catenin)↓, 1,  

Migration

5LO↓, 1,   AntiAg↓, 1,   Ca+2↝, 1,   CDK4/6↓, 1,   CLDN2↓, 1,   COL1↓, 1,   COL3A1↓, 1,   CXCL12↓, 1,   E-cadherin↓, 1,   E-cadherin↑, 2,   FAK↓, 1,   Ki-67↓, 1,   KRAS↓, 1,   LEF1↓, 1,   MMP2↓, 3,   MMP7↓, 1,   MMP9↓, 2,   MMPs↓, 4,   MSH2↑, 1,   N-cadherin↓, 1,   PDGF↓, 2,   PKCδ↓, 2,   RAGE↓, 1,   Slug↓, 1,   Snail↓, 2,   TGF-β↓, 3,   TSC1↑, 1,   TSP-1↑, 3,   TumCMig↓, 1,   TumCP↓, 1,   TumMeta↓, 1,   uPA↓, 2,   uPAR↓, 1,   Vim↓, 3,   β-catenin/ZEB1↓, 3,  

Angiogenesis & Vasculature

angioG↓, 2,   EGFR↓, 4,   Hif1a↓, 1,   NO↓, 1,   VEGF↓, 4,   VEGFR2↓, 3,  

Barriers & Transport

P-gp↓, 2,  

Immune & Inflammatory Signaling

COX2↓, 5,   CRP↓, 2,   CXCR4↓, 1,   IFN-γ↓, 1,   IKKα↓, 1,   IL10↓, 3,   IL1β↓, 1,   IL6↓, 4,   IL8↓, 1,   Inflam↓, 1,   JAK2↓, 1,   NF-kB↓, 2,   PSA↓, 1,   TLR4↓, 1,   TNF-α↓, 3,  

Hormonal & Nuclear Receptors

CDK6↓, 1,  

Drug Metabolism & Resistance

ChemoSen↑, 2,   eff↑, 11,   P450↓, 1,   selectivity↑, 2,  

Clinical Biomarkers

BRCA1↑, 1,   CRP↓, 2,   EGFR↓, 4,   HER2/EBBR2↓, 2,   IL6↓, 4,   Ki-67↓, 1,   KRAS↓, 1,   LDH↑, 1,   PSA↓, 1,   RAGE↓, 1,  

Functional Outcomes

chemoPv↑, 1,   TGFβR1↑, 1,  
Total Targets: 193

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress

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

Metal & Cofactor Biology

IronCh↓, 1,  

Core Metabolism/Glycolysis

FASN↓, 1,  

Proliferation, Differentiation & Cell State

GSK‐3β↓, 1,  

Migration

AntiAg↑, 1,  

Angiogenesis & Vasculature

angioG↓, 1,  

Immune & Inflammatory Signaling

COX2↓, 1,   IL10↓, 1,   IL17↓, 1,   IL1β↓, 1,   IL6↓, 1,   IL8↓, 1,   Inflam↓, 3,   MCP1↓, 1,   TNF-α↓, 1,  

Synaptic & Neurotransmission

tau↓, 1,  

Protein Aggregation

Aβ↓, 1,  

Drug Metabolism & Resistance

BioAv↓, 1,   Half-Life↑, 1,  

Clinical Biomarkers

BP↓, 1,   IL6↓, 1,  

Functional Outcomes

AntiCan↑, 1,   cardioP↑, 2,   neuroP↑, 1,   Pain↓, 1,  
Total Targets: 34

Scientific Paper Hit Count for: cMyc, cellular-MYC oncogene
10 Quercetin
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#:35  State#:%  Dir#:%
wNotes=0 sortOrder:rid,rpid

 

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