ArticleMedical oncology (Northwood, London, England)2025
Formononetin-induced apoptosis in hepatocellular carcinoma: insights from mTOR inhibition and caspase-3 activation through in silico and in vitro approaches.
Article in Medical oncology (Northwood, London, England), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Hepatocellular carcinoma (HCC) is the most prevalent primary liver cancer and remains a major contributor to global cancer-related deaths. The progression of HCC is strongly influenced by the dysregulation of the mechanistic target of rapamycin (mTOR) signaling pathway and impaired apoptotic mechanisms, particularly due to caspase-3 suppression. These molecular aberrations promote oncogenic proliferation and confer resistance to conventional therapeutic regimens. Existing treatment modalities are frequently constrained by limited efficacy, the emergence of drug resistance, and dose-limiting toxicities, highlighting the critical need for innovative and targeted therapeutic approaches to improve patient outcomes. This study investigates the dual anticancer mechanisms of formononetin, a bioactive isoflavone, focusing on its ability to suppress the mTOR signaling pathway and induce caspase-3 activation in hepatocellular carcinoma (HCC). By targeting these critical molecular pathways, formononetin exhibits therapeutic potential by impeding tumor progression and counteracting apoptosis resistance in HCC. In silico analyses employing molecular docking, PASS Online, and ProTox 3.0 were utilized to predict formononetin's biological activity, pharmacokinetic properties, and toxicity profile. These computational tools provided valuable insights into formononetin's potential therapeutic properties. To validate these predictions, in vitro studies were conducted, including cytotoxicity assays (MTT), apoptosis quantification via Annexin V-FITC/PI staining, and protein expression analysis of mTOR and caspase-3 using flow cytometry. The experimental results substantiated formononetin's capacity to suppress mTOR signaling and induce apoptotic cell death in HCC models. In silico analyses demonstrated that formononetin exhibited high binding affinities to mTOR (- 8.7 kcal/mol) and caspase-3 (- 7.2 kcal/mol), supported by favorable pharmacokinetic properties and low toxicity profiles. Cytotoxicity assays revealed selective activity against HepG2 cells, with an IC
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