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<p>To investigate the anti-glioblastoma potential of the natural isoflavone formononetin, focusing on its impact on cell survival, proliferation, migration, mediated through a potential mechanism involving oxidative stress modulation.&#xa0;T98G glioblastoma cells were treated with formononetin (IC<sub>30</sub> = 16.20 µM, IC<sub>50</sub> = 24.64 µM). Cytotoxicity (MTT), proliferation (trypan blue), migration (wound healing), clonogenicity (colony formation), and apoptosis (Hoechst staining) were assessed. Gene expression (qRT-PCR) of survivin, cyclin D1, Bad, MMP-9, SOD, CAT, and GPX was analyzed. Antioxidant enzyme activity and total antioxidant capacity (TAC) were measured.&#xa0;Formononetin dose-dependently reduced cell viability, proliferation, migration, and colony formation, while inducing apoptosis. It downregulated survivin, cyclin D1, MMP-9, and, unregulated Bad. Paradoxically, it significantly increased the activity of SOD, CAT, and GPX enzymes and enhanced TAC.&#xa0;Formononetin exerts potent anti-glioblastoma effects by inducing apoptosis and inhibiting key cancer hallmarks, mediated through a unique mechanism involving the paradoxical activation of the cellular antioxidant system, ultimately disrupting redox balance.</p>

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The Isoflavone Formononetin Suppresses Hallmarks of Glioblastoma Progression and Activates a Compensatory Antioxidant Pathway

  • 期刊论文

  • 发表日期：

    2025年12月11日

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  • Fatemeh Dinarvand,
  • Mehdi Salehi,
  • Seyyed Amirhossein Latifi,
  • Hadi Karami

摘要

To investigate the anti-glioblastoma potential of the natural isoflavone formononetin, focusing on its impact on cell survival, proliferation, migration, mediated through a potential mechanism involving oxidative stress modulation. T98G glioblastoma cells were treated with formononetin (IC30 = 16.20 µM, IC50 = 24.64 µM). Cytotoxicity (MTT), proliferation (trypan blue), migration (wound healing), clonogenicity (colony formation), and apoptosis (Hoechst staining) were assessed. Gene expression (qRT-PCR) of survivin, cyclin D1, Bad, MMP-9, SOD, CAT, and GPX was analyzed. Antioxidant enzyme activity and total antioxidant capacity (TAC) were measured. Formononetin dose-dependently reduced cell viability, proliferation, migration, and colony formation, while inducing apoptosis. It downregulated survivin, cyclin D1, MMP-9, and, unregulated Bad. Paradoxically, it significantly increased the activity of SOD, CAT, and GPX enzymes and enhanced TAC. Formononetin exerts potent anti-glioblastoma effects by inducing apoptosis and inhibiting key cancer hallmarks, mediated through a unique mechanism involving the paradoxical activation of the cellular antioxidant system, ultimately disrupting redox balance.