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MINI REVIEW article

Front. Cell Dev. Biol.

Sec. Epigenomics and Epigenetics

This article is part of the Research TopicEpigenetic Alterations in Tumors and Therapeutic ResistanceView all 6 articles

RBM15-mediated m6A modification in Cancer Progression and Tumor Immunity: Molecular Mechanisms and Therapeutic Potential

Provisionally accepted
  • 1Suining Central Hospital, Suining, China
  • 2City of Hope, Duarte, United States
  • 3Department of Gastroenterology, Suining Central Hospital, Suining, China

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

RBM15, a key RNA-binding protein involved in m6A RNA methylation, plays multifaceted roles in cancer development and tumor immunity. Emerging evidence indicates that RBM15 regulates tumor cell proliferation, migration, invasion, and metabolic reprogramming through modulation of RNA stability, splicing, and translation. Beyond its tumor-intrinsic effects, RBM15 influences the tumor immune microenvironment by affecting immune cell differentiation, activation, and cytokine production, thereby contributing to immune evasion. Dysregulated RBM15 expression has been observed across various cancer types, correlating with poor prognosis and therapy resistance. These findings highlight RBM15 as a promising biomarker for cancer diagnosis and prognosis and suggest its potential as a therapeutic target. Future studies focusing on RBM15-targeted interventions, either alone or in combination with immunotherapy, may provide novel strategies for precision cancer treatment.

Keywords: RBM15, RNA-Binding Protein, m6A modification, epitranscriptome, Cancer Progression, tumor immunity, biomarker, Therapeutic target

Received: 26 Sep 2025; Accepted: 19 Nov 2025.

Copyright: © 2025 Li, Jiang, Yuan and Wang. 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: Qiang Wang, wangqiang902497@126.com

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