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REVIEW article

Front. Cell Dev. Biol.

Sec. Cancer Cell Biology

Volume 13 - 2025 | doi: 10.3389/fcell.2025.1507171

Summary of the mechanism of ferroptosis regulated by m6A modification in cancer progression

Provisionally accepted
  • Bone and Soft Tissue Tumors Research Centre of Yunnan Province, Department of Orthopaedics, The Third Affiliated Hospital of Kunming Medical University (Yunnan Cancer Hospital), Kunming, China

The final, formatted version of the article will be published soon.

    The most common form of internal RNA modification in eukaryotes is called n6methyladenosine (m6A) methylation. It has become more and more well-known as a research issue in recent years since it alters RNA metabolism and is involved in numerous biological processes. Currently, m6A alteration offers new opportunities in clinical applications and is intimately linked to carcinogenesis. Ferroptosis -a form of iron-dependent, lipid peroxidation-induced regulated cell death-was discovered. In the development of cancer, it has become an important factor. According to newly available data, ferroptosis regulates tumor growth, and cancer exhibits aberrant m6A levels in crucial ferroptosis regulatory components. On the other hand, m6A has multiple roles in the development of tumors, and the relationship between m6Amodified ferroptosis and malignancies is quite intricate. In this review, we first give a thorough review of the regulatory and functional roles of m6A methylation, focusing on the molecular processes of m6A through the regulation of ferroptosis in human cancer progression and metastasis, which are strongly associated to cancer initiation, progression, and drug resistance. Therefore, it is crucial to clarify the relationship between m6A-mediated regulation of ferroptosis in cancer progression, providing a new strategy for cancer treatment with substantial clinical implications.

    Keywords: N6-Methyladenosine, m6A methyltransferases, m6A demethylase, M6A reading protein, ferroptosis, Cancer

    Received: 07 Oct 2024; Accepted: 25 Mar 2025.

    Copyright: © 2025 Fan, Chen, Huang, Li, Nabil and Yang. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

    * Correspondence: Zuozhang Yang, Bone and Soft Tissue Tumors Research Centre of Yunnan Province, Department of Orthopaedics, The Third Affiliated Hospital of Kunming Medical University (Yunnan Cancer Hospital), Kunming, China

    Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.

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