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<p>Ovarian cancer remains the most lethal gynecological malignancy, with cisplatin resistance posing a major challenge to effective treatment. Understanding the molecular mechanisms underlying this resistance is essential for developing new therapeutic strategies. In our study, RNA-seq analysis identified <i>MEF2C</i> as a differentially expressed gene (DEG) associated with the development of cisplatin resistance. This finding was validated by RT-qPCR, confirming significant differences in <i>MEF2C</i> expression between cisplatin-sensitive (A2780) and cisplatin-resistant (A2780cp) ovarian cancer cell lines. Overexpression of MEF2C in A2780cp cells led to a reduction in the IC50 of cisplatin, enhanced caspase activity, elevated levels of the pro-apoptotic nuclear receptor NR4A1 (Nur77), and a marked increase in apoptosis, as demonstrated by MTT assay, western blotting, and PI-Annexin V flow cytometry. Our findings suggest that MEF2C is downregulated in cisplatin-resistant ovarian cancer cells, and its overexpression re-sensitizes these cells to cisplatin through the activation of intrinsic apoptotic pathways. Clinically, elucidating the molecular mechanisms of chemoresistance and targeting key regulators such as MEF2C may provide a promising strategy to reprogram resistant tumor cells and enhance the efficacy of standard chemotherapy, offering a potential translational pathway toward improved therapeutic responses in ovarian cancer.</p>

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MEF2C induces intrinsic apoptosis and reverses cisplatin resistance in A2780 ovarian cancer cell line

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年11月24日

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  • Zahra Fadavi,
  • Hadi Alizadeh,
  • Seyed Javad Mowla,
  • Bahram M. Soltani

摘要

Ovarian cancer remains the most lethal gynecological malignancy, with cisplatin resistance posing a major challenge to effective treatment. Understanding the molecular mechanisms underlying this resistance is essential for developing new therapeutic strategies. In our study, RNA-seq analysis identified MEF2C as a differentially expressed gene (DEG) associated with the development of cisplatin resistance. This finding was validated by RT-qPCR, confirming significant differences in MEF2C expression between cisplatin-sensitive (A2780) and cisplatin-resistant (A2780cp) ovarian cancer cell lines. Overexpression of MEF2C in A2780cp cells led to a reduction in the IC50 of cisplatin, enhanced caspase activity, elevated levels of the pro-apoptotic nuclear receptor NR4A1 (Nur77), and a marked increase in apoptosis, as demonstrated by MTT assay, western blotting, and PI-Annexin V flow cytometry. Our findings suggest that MEF2C is downregulated in cisplatin-resistant ovarian cancer cells, and its overexpression re-sensitizes these cells to cisplatin through the activation of intrinsic apoptotic pathways. Clinically, elucidating the molecular mechanisms of chemoresistance and targeting key regulators such as MEF2C may provide a promising strategy to reprogram resistant tumor cells and enhance the efficacy of standard chemotherapy, offering a potential translational pathway toward improved therapeutic responses in ovarian cancer.