REVIEW article

Front. Immunol.

Sec. Molecular Innate Immunity

Volume 16 - 2025 | doi: 10.3389/fimmu.2025.1583039

The role of RNA methylation in glioma progression: mechanisms, diagnostic implications, and therapeutic value

Provisionally accepted
Shao-Ze  ZhangShao-Ze ZhangShao-Yan  LiuShao-Yan LiuMeng-Die  ChengMeng-Die ChengYin-Feng  ZhangYin-Feng Zhang*Jia-Wei  TianJia-Wei Tian
  • Qingdao University, Qingdao, China

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

Glioma represents a highly lethal form of malignant tumour, with RNA methylation emerging as a critical regulator of its oncogenesis and progression. As a prevalent post-translational modification, methylation influences various biological functions, particularly RNA processing, by modulating splicing, transport, and degradation of both mRNAs and noncoding RNAs. Key methylation types such as N6methyladenosine (m6A), N5-methylcytosine (m5C), N7-methylguanosine (m7G), and N1-methyladenosine (m1A) are dynamically regulated by specific enzymes known as writers, erasers, and readers. Dysregulation of these modifications contributes to glioma pathophysiology, while offering potential biomarkers for early detection and promising therapeutic targets. This review explores the mechanistic roles of RNA methylation in glioma and highlights its translational implications, aiming to advance molecular diagnostics and targeted interventions in glioma treatment.

Keywords: epitranscriptome, M6A, m5C, m7G, m1A

Received: 25 Feb 2025; Accepted: 24 Apr 2025.

Copyright: © 2025 Zhang, Liu, Cheng, Zhang and Tian. 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: Yin-Feng Zhang, Qingdao University, Qingdao, China

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