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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. -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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| Source: CGL-Driver Genes |
| Type: Oncogene |
| FMS-related tyrosine kinase 3 (FLT3) is a receptor tyrosine kinase that plays a significant role in hematopoiesis and is primarily expressed in hematopoietic stem cells and progenitor cells. It is particularly important in the context of acute myeloid leukemia (AML), where mutations in the FLT3 gene are among the most common genetic alterations. FLT3 inhibitors, such as midostaurin, gilteritinib, and quizartinib, have been developed to specifically target and inhibit the activity of the mutated FLT3 receptor. |
| 3377- | QC, | Quercetin inhibits a large panel of kinases implicated in cancer cell biology |
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#:118 State#:% Dir#:1
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