Molecular Mechanisms of Genistein in Breast Cancer: From Oxidative Stress to Oncogenic Pathway Inhibition
DOI:
https://doi.org/10.71193/jcid.20250006Keywords:
Genistein, isoflavone, oxidative stress, breast cancer, cytotoxicity, botanical sourcesAbstract
Genistein (GT), a soy-derived isoflavone, have received attention due to their possible anticancer effects. The present research is designed to explore the anticancer potential of GT in the therapeutic management of breast cancer (BC) with molecular mechanisms. For this, data have been collected from plausible different online databases, including PubMed, Web of Science, Google Scholar, PubChem, ScienceDirect, Scopus, Springer Link, and Wiley Online. The findings highlight GT’s potential to reduce oxidative damage, induce apoptosis, and modulate the cell lifecycle in BC cells. It inhibits cancer cell proliferation by affecting the human epidermal growth factor receptor 2 (HER2), phosphoinositide 3-kinase/ protein kinase B (PI3K/AKT), and hedgehog regulatory pathways. Moreover, GT exhibits promising pharmacokinetic properties, including high intestinal absorption (95.5%) and strong Caco-2 permeability, with metabolism primarily via CYP1A2 and CYP2C19. However, its poor blood-brain barrier (BBB) permeability and low water solubility present difficulties to the systemic bioavailability. Toxicological investigations demonstrate a dose-dependent effect of GT, with large dosages causing toxicity and low concentrations showing therapeutic potential. Clinical studies emphasize its complex involvement in BC, with differing findings on benefits and risks, indicating the need for additional safety and efficacy study.
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