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<p>In recent years, cancer treatment has faced significant challenges, highlighting the urgent need for novel therapeutic strategies. Ferroptosis is a regulated type of cellular demise that is distinguished by lipid peroxidation reliant on iron. This process has been recognized as a significant mechanism involved in both the suppression and progression of tumors. A growing body of evidence suggests that ferroptosis is intricately governed by epigenetic processes, which encompass modifications to RNA that occur after transcription. mong the various RNA modifications, N6-methyladenosine (m6A) stands out as the most thoroughly investigated and is pivotal in regulating gene expression pathways linked to the sensitivity of tumor cells to ferroptosis. Furthermore, recent research indicates that additional RNA modifications, including m1A, m5C, m7G, ac4C and A to I editing might also be involved in the regulation of ferroptosis; however, the existing evidence is still scarce and primarily exploratory in nature. In this review, we provide an integrated overview of m6A-centered regulatory mechanisms of ferroptosis in cancer, while also summarizing recent advances and knowledge gaps regarding less-characterized RNA modifications. We also We further discuss how RNA modification–mediated regulation of ferroptosis intersects with tumor progression and therapeutic resistance. By highlighting both established mechanisms and underexplored areas, this review aims to identify potential therapeutic targets and outline future directions for exploiting ferroptosis in cancer treatment.</p>

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RNA modifications and cancer ferroptosis

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年3月28日

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  • Yingda Xie,
  • Bo Sun,
  • Wenjuan Chen,
  • Xueying Jia,
  • Yitao Fan,
  • Ziyi Xu,
  • Hongyan Liu,
  • Xinyu Gu,
  • Fuqiang Ma

摘要

In recent years, cancer treatment has faced significant challenges, highlighting the urgent need for novel therapeutic strategies. Ferroptosis is a regulated type of cellular demise that is distinguished by lipid peroxidation reliant on iron. This process has been recognized as a significant mechanism involved in both the suppression and progression of tumors. A growing body of evidence suggests that ferroptosis is intricately governed by epigenetic processes, which encompass modifications to RNA that occur after transcription. mong the various RNA modifications, N6-methyladenosine (m6A) stands out as the most thoroughly investigated and is pivotal in regulating gene expression pathways linked to the sensitivity of tumor cells to ferroptosis. Furthermore, recent research indicates that additional RNA modifications, including m1A, m5C, m7G, ac4C and A to I editing might also be involved in the regulation of ferroptosis; however, the existing evidence is still scarce and primarily exploratory in nature. In this review, we provide an integrated overview of m6A-centered regulatory mechanisms of ferroptosis in cancer, while also summarizing recent advances and knowledge gaps regarding less-characterized RNA modifications. We also We further discuss how RNA modification–mediated regulation of ferroptosis intersects with tumor progression and therapeutic resistance. By highlighting both established mechanisms and underexplored areas, this review aims to identify potential therapeutic targets and outline future directions for exploiting ferroptosis in cancer treatment.