ArticleBMC medical genomics2025
m6A regulator-based molecular classification and hub genes associated with immune infiltration characteristics and clinical outcomes in diffuse gliomas.
Article in BMC medical genomics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Identification of a novel m6A RNA methylation regulator-based signature for prognosis and immune landscape prediction in hepatocellular carcinoma.Scientific reports · 2025Article
- Multi-omics insights into the role of mitophagy receptor-related genes in glioma prognosis and immune microenvironment remodeling.Frontiers in immunology · 2025Article
- The long pentraxin 3: the invisible loom weaving the warp and weft of tumor destiny.Frontiers in immunology · 2025Review
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6 authors.
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Abstract
backgroundm6A methylation modification is a new regulatory mechanism involved in tumorigenesis and tumor-immunity interaction. However, its impact on glioma immune microenvironment and clinical outcomes remains unclear.
methodsComprehensive expression profiles of 18 m6A regulators were used to identify molecular subtypes exhibiting distinct m6A modification patterns in 1673 glioma samples sourced from public datasets. A multi-genes signature was constructed for predicting clinical outcomes and response to immunotherapy in glioma patients. Immunohistochemistry and cellular experiments were performed for validation.
resultsTwo m6A subtypes of gliomas were identified. The m6A-low-risk subtype was characterized by paucity of immune infiltrates; While the m6A-high-risk subtype had higher abundances of multiple immune cells including lymphocyte and macrophage as well as increased expression of PD-L1, corresponding to an immunosuppressive phenotype. The m6A-high-risk subtype had poorer survival than the m6A-low-risk subtype in both the glioblastoma and lower grade gliomas cohorts. Eight m6A-related hub genes of high prognostic significances were identified and selected for developing a scoring signature termed as m6Ascore. Elevated m6Ascore indicated worse survival for glioma patients under standard care, but showed enhanced response to immunotherapy. Moreover, we demonstrated that overexpression of FTO, a m6A demethylase, inhibited the expressions of m6A-related hub genes (PTX3, SPAG4), impaired glioma cell viability and reduced macrophage chemotaxis.
conclusionThis work develops an immune- and clinical-relevant m6A subtyping and a scoring model, which enhances our understanding of the role of m6A modification in regulating immune infiltration microenvironment in gliomas and helps to identify patients who are more likely to benefit from immunotherapy.
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