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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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| Source: |
| Type: white blood cell |
| T cells are white blood cells that play a central role in the adaptive immune response. Subsets and Function: Cytotoxic T Cells (CD8+): Recognize and kill infected or malignant cells. Helper T Cells (CD4+): Assist in orchestrating the immune response by secreting cytokines and supporting the functions of other immune cells. T cells, particularly CD8+ cytotoxic T cells, can recognize tumor antigens presented on major histocompatibility complex (MHC) molecules and directly kill malignant cells. Regulatory T Cells (Tregs): Maintain immune tolerance and prevent autoimmunity but may also suppress anti-tumor responses in the tumor microenvironment. Tumor-Infiltrating Lymphocytes (TILs): Tumor Microenvironment: The presence of T cells within tumors, often referred to as tumor-infiltrating lymphocytes, is a key indicator of an ongoing anti-tumor immune response. Regulatory T Cells (Tregs): Tregs within the tumor environment may inhibit the activity of cytotoxic T cells through the secretion of immunosuppressive cytokines (e.g., IL-10, TGF-β), thus allowing tumors to evade the immune response. In many cancers, a robust T cell infiltrate is correlated with a better overall survival, lower rates of relapse, and improved responses to therapy. Assessing the type, density, and activation state of T cells in the tumor microenvironment can provide valuable prognostic information. High levels of active, cytotoxic T cells generally indicate a better prognosis. |
| 871- | RES, | CUR, | QC, | The effect of resveratrol, curcumin and quercetin combination on immuno-suppression of tumor microenvironment for breast tumor-bearing mice |
| - | in-vitro, | BC, | 4T1 | - | in-vivo, | BC, | 4T1 |
| 103- | RES, | CUR, | QC, | The effect of resveratrol, curcumin and quercetin combination on immuno-suppression of tumor microenvironment for breast tumor-bearing mice |
| - | vitro+vivo, | BC, | 4T1 |
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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