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<p>Cisplatin is one of the most widely used chemotherapeutic drugs in treating malignant tumors. However, its clinical efficacy is severely compromised by the emergence of drug resistance. Recent studies have highlighted N6-methyladenosine (m6A) modification, a key epigenetic regulatory mechanism, as playing a crucial role in the development of cisplatin resistance. m6A modification regulates essential RNA processes, including RNA stability, translation efficiency, and subcellular localization, through the coordinated activities of “writers” (e.g., METTL3, WTAP), “erasers” (e.g., FTO, ALKBH5), and “readers” (e.g., YTH family, GF2BPfamily). These regulatory effects ultimately affect cancer cell sensitivity to cisplatin. Furthermore, m6A modification is critically involved in the regulation of fundamental cellular processes such as autophagy, apoptosis, and tumor metabolism, thereby contributing to the reinforcement of resistance mechanisms. This review provides a comprehensive summary of the mechanisms through which m6A modification mediates cisplatin resistance and discusses its potential implications for precision cancer therapy. This review consolidates the scientific foundation for potential future strategies and innovative approaches targeting chemoresistance.</p>

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Decoding drug resistance: the role of m6A modification in cisplatin efficacy

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年4月1日

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  • Zile Zhang,
  • HanBin Qin,
  • Jiaxin Sui,
  • Chunru Xu,
  • Kaixin Liu,
  • Xin Zhao,
  • Zhonglu Liu,
  • Hua Zhang,
  • Xuexia Liu

摘要

Cisplatin is one of the most widely used chemotherapeutic drugs in treating malignant tumors. However, its clinical efficacy is severely compromised by the emergence of drug resistance. Recent studies have highlighted N6-methyladenosine (m6A) modification, a key epigenetic regulatory mechanism, as playing a crucial role in the development of cisplatin resistance. m6A modification regulates essential RNA processes, including RNA stability, translation efficiency, and subcellular localization, through the coordinated activities of “writers” (e.g., METTL3, WTAP), “erasers” (e.g., FTO, ALKBH5), and “readers” (e.g., YTH family, GF2BPfamily). These regulatory effects ultimately affect cancer cell sensitivity to cisplatin. Furthermore, m6A modification is critically involved in the regulation of fundamental cellular processes such as autophagy, apoptosis, and tumor metabolism, thereby contributing to the reinforcement of resistance mechanisms. This review provides a comprehensive summary of the mechanisms through which m6A modification mediates cisplatin resistance and discusses its potential implications for precision cancer therapy. This review consolidates the scientific foundation for potential future strategies and innovative approaches targeting chemoresistance.