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| 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
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| Caspase-10 is a member of the caspase family of cysteine proteases, which play essential roles in programmed cell death (apoptosis) and inflammation. Caspase-10 is crucial for the induction of apoptosis in response to various signals. In many cancers, the apoptotic pathways are dysregulated, allowing cancer cells to evade programmed cell death. Loss of caspase-10 function or expression can contribute to this evasion, promoting tumor survival and growth. Caspase-10 may act as a tumor suppressor. Its expression can be downregulated in various cancers, including breast, colorectal, and prostate cancers. Caspase-10 is frequently downregulated in various cancers, which may contribute to the evasion of apoptosis and tumor progression. |
| 923- | QC, | Quercetin as an innovative therapeutic tool for cancer chemoprevention: Molecular mechanisms and implications in human health |
| - | Review, | Var, | NA |
| 48- | QC, | Quercetin Potentiates Apoptosis by Inhibiting Nuclear Factor-kappaB Signaling in H460 Lung Cancer Cells |
| - | in-vitro, | NSCLC, | H460 |
| 86- | QC, | PacT, | Quercetin regulates insulin like growth factor signaling and induces intrinsic and extrinsic pathway mediated apoptosis in androgen independent prostate cancer cells (PC-3) |
| - | vitro+vivo, | Pca, | PC3 |
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
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