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REVIEW article
Front. Cell Dev. Biol.
Sec. Cancer Cell Biology
Volume 13 - 2025 | doi: 10.3389/fcell.2025.1539678
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Metastasis remains a primary cause of cancer-related mortality, with its intricate mechanisms continuing to be uncovered through advancing research. Among the various regulatory processes involved, RNA modification has emerged as a critical epitranscriptomic mechanism influencing cancer metastasis. N6-methyladenosine (m6A), recognized as one of the most prevalent and functionally significant RNA modifications, plays a central role in the regulation of RNA metabolism. In this review, we explore the multifaceted role of m6A in the different stages of cancer metastasis, including epithelial-mesenchymal transition, invasion, migration, and colonization. In addition to summarizing the current state of our understanding, we offer insights into how m6A modifications modulate key oncogenic pathways, highlighting the implications of recent discoveries for therapeutic interventions. Furthermore, we critically assess the limitations of previous studies and propose areas for future research, including the potential for targeting m6A as a novel approach in anti-metastatic therapies. Our analysis provides a comprehensive understanding of the regulatory landscape of m6A in metastasis, offering directions for continued exploration in this rapidly evolving field.
Keywords: M6A, RNA, Methylation, metastasis, Cancer
Received: 04 Dec 2024; Accepted: 16 Apr 2025.
Copyright: © 2025 Zhou, Cao and Qing. 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: Zhu Qing, West China Hospital, Sichuan University, Chengdu, 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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