Quercetin / CRP 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


CRP, C-reactive protein: Click to Expand ⟱
Source:
Type:
C-Reactive Protein (CRP) is a protein produced by the liver in response to inflammation in the body.
C-reactive protein is an acute-phase reactant synthesized by the liver in response to IL-6–driven inflammation.

In oncology, it serves as a host-response biomarker, not a tumor marker.

An elevated CRP integrates multiple cancer-relevant processes:
-Tumor-associated inflammation and necrosis
-Cytokine signaling (especially IL-6)
-Infection or treatment-related tissue injury
-Cachexia and systemic catabolism

Because it aggregates these signals, CRP is a powerful global severity indicator.

Prognosis (Primary Use)
-Higher baseline CRP correlates with shorter overall survival across many cancers.
-Rising CRP often precedes clinical decline.

Treatment Tolerance & Risk
-Elevated CRP predicts poor chemotherapy tolerance, higher complication rates, and inferior immunotherapy outcomes in several settings.


Scientific Papers found: Click to Expand⟱
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↓,
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↓, *Aβ↓,
3347- QC,    Recent Advances in Potential Health Benefits of Quercetin
- Review, Var, NA - Review, AD, NA
*antiOx↑, *ROS↓, *Inflam↓, TumCP↓, Apoptosis↑, *cardioP↑, *BP↓, TumMeta↓, MDR1↓, NADPH↓, ChemoSen↑, MMPs↓, TIMP2↑, *NLRP3↓, *IFN-γ↑, *COX2↓, *NF-kB↓, *MAPK↓, *CRP↓, *IL6↓, *TNF-α↓, *IL1β↓, *TLR4↑, *PKCδ↓, *AP-1↓, *ICAM-1↓, *NRF2↑, *HO-1↑, *lipid-P↓, *neuroP↑, *eff↑, *memory↑, *cognitive↑, *AChE↓, *BioAv↑, *BioAv↑, *BioAv↑, *BioAv↑, *BioAv↑,
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↑,

Showing Research Papers: 1 to 4 of 4

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 4

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress

GSH↑, 1,   MDA↓, 1,   NRF2↑, 1,   ROS↓, 1,   ROS↑, 1,   SOD↑, 1,  

Mitochondria & Bioenergetics

EGF↓, 1,   FGFR1↓, 1,   Raf↓, 1,  

Core Metabolism/Glycolysis

cMyc↓, 2,   LDH↑, 1,   NADPH↓, 1,  

Cell Death

Akt↓, 2,   Apoptosis↑, 2,   Bak↑, 1,   BAX↑, 1,   Bcl-2↓, 1,   Casp3↓, 1,   Casp9↑, 1,   cFLIP↓, 1,   Cyt‑c↑, 1,   DR5↑, 1,   FasL↑, 1,   MAPK↓, 1,   MAPK↑, 1,   p38↑, 1,  

Kinase & Signal Transduction

HER2/EBBR2↓, 1,  

Transcription & Epigenetics

miR-21↑, 1,   p‑pRB↓, 1,  

Protein Folding & ER Stress

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

Autophagy & Lysosomes

Beclin-1↑, 1,   LC3B-II↑, 1,  

DNA Damage & Repair

P53↑, 1,   PARP↓, 1,  

Cell Cycle & Senescence

CDK1↓, 1,   CDK2↑, 1,   CycB/CCNB1↓, 1,   cycD1/CCND1↓, 2,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State

CSCs↓, 1,   Diff↓, 1,   EMT↓, 1,   ERK↑, 1,   FGF↓, 1,   IGFBP3↑, 1,   mTOR↓, 2,   NOTCH↓, 1,   PI3K↓, 2,   RAS↓, 1,   Shh↓, 1,   STAT↓, 1,   STAT3↓, 1,   p‑STAT3↓, 1,   STAT4↓, 1,   Wnt↓, 1,  

Migration

FAK↓, 1,   MMP2↓, 2,   MMP9↓, 1,   MMPs↓, 2,   PDGF↓, 1,   TGF-β↓, 1,   TIMP2↑, 1,   TSP-1↑, 1,   TumCP↓, 2,   TumMeta↓, 1,   uPA↓, 1,   uPAR↓, 1,  

Angiogenesis & Vasculature

angioG↓, 1,   EGFR↓, 1,   NO↓, 1,   VEGF↓, 1,   VEGFR2↓, 1,  

Immune & Inflammatory Signaling

COX2↓, 3,   CRP↓, 3,   IL10↓, 2,   IL1β↓, 1,   IL6↓, 2,   Inflam↓, 1,   JAK↓, 1,   JAK2↓, 1,   NF-kB↓, 1,   TLR4↓, 1,   TNF-α↓, 1,  

Drug Metabolism & Resistance

ChemoSen↑, 1,   MDR1↓, 1,   selectivity↑, 1,  

Clinical Biomarkers

CRP↓, 3,   EGFR↓, 1,   HER2/EBBR2↓, 1,   IL6↓, 2,   LDH↑, 1,  
Total Targets: 94

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress

antiOx↑, 1,   HO-1↑, 1,   lipid-P↓, 1,   NRF2↑, 1,   ROS↓, 1,  

Cell Death

MAPK↓, 1,  

Migration

AP-1↓, 1,   PKCδ↓, 1,  

Immune & Inflammatory Signaling

COX2↓, 1,   CRP↓, 1,   ICAM-1↓, 1,   IFN-γ↑, 1,   IL1β↓, 2,   IL6↓, 2,   Inflam↓, 1,   NF-kB↓, 1,   TLR4↑, 1,   TNF-α↓, 2,  

Synaptic & Neurotransmission

AChE↓, 1,  

Protein Aggregation

Aβ↓, 1,   NLRP3↓, 1,  

Drug Metabolism & Resistance

BioAv↑, 5,   eff↑, 2,  

Clinical Biomarkers

BP↓, 1,   CRP↓, 1,   IL6↓, 2,  

Functional Outcomes

cardioP↑, 1,   cognitive↑, 1,   memory↑, 1,   neuroP↑, 2,  
Total Targets: 30

Scientific Paper Hit Count for: CRP, C-reactive protein
4 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#:884  State#:%  Dir#:1
wNotes=0 sortOrder:rid,rpid

 

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