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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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| Endonucleases are enzymes that play a crucial role in the maintenance of genome stability by cleaving the phosphodiester backbone of DNA. In the context of cancer, endonucleases can have both tumor-suppressing and tumor-promoting effects. 1. APEX1 (Apurinic/Apyrimidinic Endonuclease 1) Cancers: Breast cancer, lung cancer, colorectal cancer Prognosis: High expression is often associated with poor prognosis due to its role in DNA repair and resistance to chemotherapy. 2. FEN1 (Flap Endonuclease 1) Cancers: Breast cancer, prostate cancer, pancreatic cancer Prognosis: Overexpression is linked to increased tumor aggressiveness and poor survival rates. 3. EXO1 (Exonuclease 1) Cancers: Colorectal cancer, ovarian cancer Prognosis: High levels of EXO1 expression can correlate with poor prognosis and increased risk of metastasis. 4. DNase I (Deoxyribonuclease I) Cancers: Various solid tumors Prognosis: Altered expression levels can be indicative of tumor progression and immune evasion. 5. Caspase-3 (an endonuclease involved in apoptosis) Cancers: Various cancers, including leukemia and solid tumors Prognosis: High levels of active caspase-3 are often associated with increased apoptosis and may correlate with better treatment responses. 6. Rad51 (a recombinase with endonuclease activity) Cancers: Breast cancer, ovarian cancer Prognosis: Elevated expression is often linked to resistance to DNA-damaging therapies and poor prognosis. 7. MRE11 (part of the MRN complex) Cancers: Breast cancer, lung cancer Prognosis: Altered expression can indicate defects in DNA repair mechanisms, influencing treatment outcomes. 8. TDP1 (Tyrosyl-DNA Phosphodiesterase 1) Cancers: Glioblastoma, breast cancer Prognosis: High expression levels may be associated with resistance to certain chemotherapeutic agents. 9. UNG (Uracil-DNA Glycosylase) Cancers: Colorectal cancer, lung cancer Prognosis: Its expression can influence the mutation rate and may correlate with tumor aggressiveness. 10. LIG3 (DNA Ligase III) Cancers: Various cancers, including breast and prostate cancer Prognosis: Overexpression may be linked to enhanced DNA repair capabilities, contributing to treatment resistance. |
| 3374- | QC, | Therapeutic effects of quercetin in oral cancer therapy: a systematic review of preclinical evidence focused on oxidative damage, apoptosis and anti-metastasis |
| - | Review, | Oral, | NA | - | Review, | AD, | NA |
| 3372- | QC, | FIS, | KaempF, | Anticancer Potential of Selected Flavonols: Fisetin, Kaempferol, and Quercetin on Head and Neck Cancers |
| - | Review, | HNSCC, | NA |
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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