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Purpose  Glioblastoma multiforme (GBM) is a common and aggressive form of brain tumor. The N 6 -methyladenosine (m 6 A) mRNA modification plays multiple roles in many biological processes and disease states. However, the relationship between m 6 A modifications and the tumor microenvironment in GBM remains unclear, especially at the single-cell level.    Experimental Design  Single-cell and bulk RNA-sequencing data were acquired from the GEO and TCGA databases, respectively. We used bioinformatics and statistical tools to analyze associations between m 6 A regulators and multiple factors.    Results   HNRNPA2B1  and  HNRNPC  were extensively expressed in the GBM microenvironment. m 6 A regulators promoted the stemness state in GBM cancer cells. Immune-related BP terms were enriched in modules of m 6 A-related genes. Cell communication analysis identified genes in the GALECTIN signaling network in GBM samples, and expression of these genes ( LGALS9 ,  CD44 ,  CD45 , and  HAVCR2 ) correlated with that of m 6 A regulators. Validation experiments revealed that  MDK  in MK signaling network promoted migration and immunosuppressive polarization of macrophage. Expression of m 6 A regulators correlated with ICPs in GBM cancer cells, M2 macrophages and T/NK cells. Bulk RNA-seq analysis identified two expression patterns (low m 6 A/high ICP and high m 6 A/low ICP) with different predicted immune infiltration and responses to ICP inhibitors. A predictive nomogram model to distinguish these 2 clusters was constructed and validated with excellent performance.    Conclusion  At the single-cell level, m 6 A modification facilitates the stemness state in GBM cancer cells and promotes an immunosuppressive microenvironment through ICPs and the GALECTIN signaling pathway network. And we also identified two m 6 A-ICP expression patterns. These findings could lead to novel treatment strategies for GBM patients.

Roles of the m6A Modification of RNA in the Glioblastoma Microenvironment as Revealed by Single-Cell Analyses