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Review
. 2023 Dec 11;28(1):103.
doi: 10.1186/s11658-023-00514-0.

Role of N6-methyladenosine methylation in glioma: recent insights and future directions

Chunlin Li #  1 , Bowen Li #  2 , Hui Wang  3 , Linglong Qu  2 , Hui Liu  4 , Chao Weng  5   6 , Jinming Han  7 , Yuan Li  8   9
Affiliations
Review

Role of N6-methyladenosine methylation in glioma: recent insights and future directions

Chunlin Li et al. Cell Mol Biol Lett. .

Abstract

Glioma is the most pervasive intracranial tumor in the central nervous system (CNS), with glioblastoma (GBM) being the most malignant type having a highly heterogeneous cancer cell population. There is a significantly high mortality rate in GBM patients. Molecular biomarkers related to GBM malignancy may have prognostic values in predicting survival outcomes and therapeutic responses, especially in patients with high-grade gliomas. In particular, N6-methyladenine (m6A) mRNA modification is the most abundant form of post-transcriptional RNA modification in mammals and is involved in regulating mRNA translation and degradation. Cumulative findings indicate that m6A methylation plays a crucial part in neurogenesis and glioma pathogenesis. In this review, we summarize recent advances regarding the functional significance of m6A modification and its regulatory factors in glioma occurrence and progression. Significant advancement of m6A methylation-associated regulators as potential therapeutic targets is also discussed.

Keywords: Glioma; N6-methyladenosine methylation; Neurogenesis; RNA.

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Conflict of interest statement

The authors have declared that no competing interest exists.

Figures

Fig. 1
Fig. 1
Dynamic and reversible processes of m6A methylation modifications. The m6A modification is primarily catalyzed by a methyltransferase complex, including METTL3, METTL14, WTAP, ZC3H13, etc. Demethylase FTO or ALKBH5 removes the m6A modification from the target mRNA. Reader proteins recognize m6A methylation and determine target mRNA fate
Fig. 2
Fig. 2
Example of functional m6A methylation-related regulators in cancers. M6A modification is a potential part of cancer progression by regulating the expression of tumor-related genes. M6A modification promotes cancer progression by enhancing the oncogene expression and inhibiting tumor-suppressor gene expression. M6A modification suppresses cancer progression by inhibiting oncogene expression while enhancing tumor-suppressor gene expression
Fig. 3
Fig. 3
M6A methylation-related regulators in glioma. Regulatory factors of m6A methylation affect the growth, self-renewal, proliferation, differentiation, autophagy, apoptosis, migration, invasion, drug resistance, and immunosuppression of glioma stem cells (GSCs) through various cellular pathways to regulate the occurrence and development of gliomas
See this image and copyright information in PMC

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