| Features: Estrogen-like activity | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Genistein is a naturally occurring isoflavone predominantly found in soy products. It binds estrogen receptors (with relative preference for ERβ over ERα), inhibits certain tyrosine kinases, and modulates PI3K/AKT, NF-κB, MAPK, and cell-cycle pathways in preclinical cancer models. It is also reported to influence angiogenesis and epigenetic regulation. Oral exposure produces conjugated metabolites (glucuronides/sulfates), and free genistein plasma levels are typically much lower than many in-vitro µM concentrations. -soy isoflavone Anticancer effects through several mechanisms: -Modulation of Hormone Activity: can bind to estrogen receptors(hormone-dependent cancers like breast and prostate cancer). -Inhibition of Cell Proliferation:- -inducing cell cycle arrest. -Induction of Apoptosis:- by influencing pro- and anti-apoptotic regulators. -Anti-inflammatory and Antioxidant Effects:-antioxidant properties help to neutralize ROS -Anti-angiogenic Activity:may also inhibit tumor angiogenesis Key Cellular Signaling Pathways Involved -Estrogen Receptor Signaling: interacting with estrogen receptors (ERα and ERβ) -PI3K/Akt/mTOR Pathway:inhibits this pro-survival pathway, leading to reduced cell growth -MAPK/ERK Pathway: can contribute to cell cycle arrest. -NF-κB Pathway:may downregulate NF-κB, supporting a reduction in tumor-promoting inflammation. -Wnt/β-catenin Pathway: involved in cell proliferation, differentiation, and oncogenic transformation. Dosages often ranging from approximately 40 mg to 100 mg per day for potential therapeutic effects. Genistein has limited bioavailability when ingested as part of the diet. Efforts to enhance its absorption include the use of specific formulations, such as those that combine genistein with other compounds or utilize novel delivery systems.
Time-Scale Flag (TSF): P / R / G
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| Enzymes involved in regulating gene expression by removing acetyl groups from histones, the proteins around which DNA is wrapped. -Many cancers exhibit altered expression levels of HDACs, which can contribute to the dysregulation of genes involved in cell growth, survival, and differentiation. -HDACs can repress the expression of tumor suppressor genes, leading to uncontrolled cell proliferation and survival. This repression can be a key factor in the development and progression of cancer. -HDAC inhibitors (HDACi) have been developed and are being investigated for their ability to reactivate silenced genes, induce cell cycle arrest, and promote apoptosis in cancer cells. -HDAC1, HDAC2): Often overexpressed in various cancers, including breast, prostate, and colorectal cancers. Their overexpression is associated with poor prognosis. -HDAC4, HDAC5): These may have both oncogenic and tumor-suppressive roles depending on the context and cancer type. -While HDACs are not classified as traditional oncogenes, their overexpression and activity can contribute to oncogenic processes. -HDAC inhibitor works by preventing the removal of acetyl groups from histones, thereby modulating gene expression, influencing cell behavior, and potentially reversing aberrant gene silencing seen in various diseases. -HDAC inhibitors can help reactivate these genes, thereby inhibiting growth and inducing apoptosis in cancer cells. |
| 1435- | GEN, | SFN, | The Effects of Combinatorial Genistein and Sulforaphane in Breast Tumor Inhibition: Role in Epigenetic Regulation |
| - | in-vitro, | BC, | MDA-MB-231 | - | in-vitro, | BC, | MCF-7 |
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#:85 Target#:140 State#:% Dir#:1
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