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| Chrysin is found in passion flower and honey. It is a flavonoid. -To reach plasma levels that might more closely match the concentrations used in in vitro studies (typically micromolar), considerably high doses or advanced delivery mechanisms would be necessary. Chrysin is widely summarized as modulating PI3K/Akt and MAPK pathways in cancer. Chrysin — Chrysin is a naturally occurring flavone-class flavonoid found in honey, propolis, passionflower, and several plants. Its oncology relevance is mainly preclinical: it shows multi-pathway anticancer activity in cell and animal models, but native oral chrysin has very poor systemic bioavailability and no established approved oncology use. Primary mechanisms (ranked):
Bioavailability / PK relevance: Native oral chrysin has very poor systemic exposure because of low aqueous solubility, extensive intestinal/hepatic glucuronidation and sulfation, and efflux; human oral bioavailability has been reported as extremely low, often summarized as below 1%. Formulation strategies such as nanoparticles, lipid systems, micelles, cyclodextrins, or structural analogues are commonly proposed for systemic translation. In-vitro vs systemic exposure relevance: Most anticancer studies use micromolar in-vitro concentrations that are unlikely to be reached in plasma after ordinary oral chrysin. Local intestinal exposure may be more plausible than systemic tumor exposure, but systemic anticancer claims should be treated as formulation-dependent. Clinical evidence status: Preclinical. Evidence is strong enough for mechanistic oncology interest in cell and animal models, including combination/sensitization studies, but there is no mature clinical oncology evidence establishing therapeutic benefit. -Note half-life 2 hrs, BioAv very poor often <1%Pathways: Graphical Pathways - may induce ROS production - ROS↑ related: MMP↓(ΔΨm), ER Stress↑, UPR↑, GRP78↑, Ca+2↑, Cyt‑c↑, Caspases↑, DNA damage↑, cl-PARP↑, HSP↓ - May Lower AntiOxidant defense in Cancer Cells: NRF2↓, GSH↓ HO1↓ - May Raise AntiOxidant defense in Normal Cells: ROS↓, NRF2↑, SOD↑, GSH↑, Catalase↑, - lowers Inflammation : NF-kB↓, COX2↓, Pro-Inflammatory Cytokines : IL-1β↓, TNF-α↓, IL-6↓, - inhibit Growth/Metastases : TumMeta↓, TumCG↓, EMT↓, MMP2↓, MMP9↓, TIMP2, uPA↓, VEGF↓, ROCK1↓, FAK↓, RhoA↓, NF-κB↓, ERK↓ - reactivate genes thereby inhibiting cancer cell growth : HDAC↓, P53↑, HSP↓, - cause Cell cycle arrest : TumCCA↑, cyclin D1↓, CDK2↓, CDK4↓, - inhibits Migration/Invasion : TumCMig↓, TumCI↓, FAK↓, ERK↓, EMT↓, TOP1↓, TET1↓, - inhibits glycolysis and ATP depletion : HIF-1α↓, cMyc↓, GLUT1↓, LDH↓, HK2↓, PDKs↓, HK2↓, GRP78↑, GlucoseCon↓ - inhibits angiogenesis↓ : VEGF↓, HIF-1α↓, Notch↓, PDGF↓, EGFR↓, - Others: PI3K↓, AKT↓, STAT↓, Wnt↓, AMPK↓, ERK↓, JNK, TrxR, - Synergies: chemo-sensitization, chemoProtective, RadioSensitizer, Others(review target notes), Neuroprotective, Cognitive, Renoprotection, Hepatoprotective, CardioProtective, - Selectivity: Cancer Cells vs Normal Cells Chrysin Mechanistic Profile
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| uPA (urokinase plasminogen activator) is a serine protease that plays a crucial role in the conversion of plasminogen to plasmin, an enzyme responsible for degrading various components of the extracellular matrix (ECM). This activity is central to processes such as tissue remodeling, cell migration, and angiogenesis. In the context of cancer, uPA facilitates tumor invasion and metastasis by promoting ECM degradation, while its interaction with its receptor (uPAR) and inhibitors (such as PAI-1) forms a regulatory axis that is frequently dysregulated in malignancies. Patients with higher pretreatment serum uPA (≥1 ng/ml) had significantly shorter OS. Elevated uPA expression has been observed in a broad range of cancers, including breast, colorectal, lung, and prostate cancers. These high levels are often indicative of increased proteolytic activity within the tumor microenvironment. Tumors with aggressive behavior often exhibit upregulation of uPA, along with its receptor uPAR. This upregulation enhances plasmin generation and leads to an environment conducive to invasion and metastasis. Elevated uPA levels in tumor tissues have been strongly associated with poor clinical outcomes. High uPA expression is correlated with increased risk of metastasis, higher likelihood of recurrence, and reduced overall survival in several cancer types. |
| 2781- | CHr, | PBG, | Chrysin a promising anticancer agent: recent perspectives |
| - | Review, | Var, | 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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