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REVIEW ARTICLE

N6-methyladenosine: A pivotal regulator in glioma oncogenesis and progression

Jingjing Li1 ,  Xiaoguang Zhang2 ,  Yaoyao Wang1 ,  Chen Dong1 ,  Haotian Li1 ,  Ying Wang3* ,  Shuangyu Lv1,2,4*
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1 Henan International Joint Laboratory for Nuclear Protein Regulation, School of Basic Medical Sciences, Henan University, Kaifeng, Henan, China
2 Department of Neurosurgery, The First Affiliated Hospital of Henan University, Henan University, Kaifeng, Henan, China
3 Department of Anesthesiology, The First Affiliated Hospital of Henan University, Henan University, Kaifeng, Henan, China
4 The Zhongzhou Laboratory for Integrative Biology, Henan University, Zhengzhou, Henan, China
GPD, 025400073 https://doi.org/10.36922/GPD025400073
Received: 1 October 2025 | Revised: 16 December 2025 | Accepted: 26 December 2025 | Published online: 19 January 2026
© 2026 by the Author(s). This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution 4.0 International License ( https://creativecommons.org/licenses/by/4.0/ )
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Abstract

Gliomas are the most prevalent primary neoplasms of the central nervous system and arise from glial cells present in the brain or spinal cord. N6-methyladenosine (m6A) is one of the most frequently occurring modifications in RNA, and its potential implications in glioma have received widespread attention in recent years. In glioma, m6A-related enzymes are capable of modifying target RNAs, influencing their translation, degradation, and splicing, which can promote or inhibit biological processes such as ferroptosis and glycolysis, ultimately impacting the progression of glioma. Furthermore, upstream modulators are capable of regulating the expression of m6A-associated enzymes, ultimately affecting glioma development by modulating m6A modification on target RNAs. In addition, the m6A modification influences glioma resistance to temozolomide, resulting in an impact on glioma patient survival. This review comprehensively delineates the molecular mechanisms by which m6A and its upstream signaling molecules regulate glioma development, emphasizing their potential value in exploring new therapeutic approaches and improving patient prognosis.

Keywords
Glioma
N6-methyladenosine
Epigenetic and transcriptomic modifications
Molecular mechanism
Funding
This work was supported by the Medical Science and Technology Program of Henan Province (no. JQRC2025017, no. SBGJ202502086, and no. SBGJ202502084), the Key Scientific Research Program for Universities of Henan Province (no. 26A320003), the Key Science and Technology Program of Henan Province in China (no. 242102310274), the Open Project Research of the First Affiliated Hospital of Henan University (no. KFZD25005), the Program for Innovative Talents of Science and Technology in Henan Province (no. 23HASTIT043), the China Postdoctoral Science Fundation (no. 2024M750782), the Youth Promotion Project of Zhongzhou Laboratory for Integrative Biology (no. 2024TS0202), and the Open Project of The First Affiliated Hospital of Henan University (no. KFMS25004).
Conflict of interest
Shuangyu Lv is an Editorial Board Member of this journal, but was not in any way involved in the editorial and peer-review process conducted for this paper, directly or indirectly. Separately, other authors declared that they have no known competing financial interests or personal relationships that could have influenced the work reported in this paper.
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Gene & Protein in Disease, Electronic ISSN: 2811-003X Published by AccScience Publishing
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