ArticleDiscover oncology2026
RBM43 promotes glioma aggressiveness and shapes the immune microenvironment through macrophage polarization.
Article in Discover oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
objectiveTo investigate the expression pattern of RBM43 in glioma and evaluate its prognostic significance, with particular attention to its association with the glioma immune microenvironment.
methodsRBM43 expression, clinicopathological associations, and prognostic value were analyzed using RNA-seq data from the TCGA and GTEx databases. RBM43 function was evaluated in vitro using proliferation, migration, and apoptosis assays, and was further tested in an in vivo mouse model. To probe RBM43-related biology, Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and Gene Set Enrichment Analysis (GSEA) were performed to identify enriched pathways. Immune infiltration and macrophage polarization were assessed using immune-related bioinformatic analyses and flow cytometry with M1/M2 markers.
resultsElevated RBM43 expression in glioma correlated with higher WHO grade, IDH-wildtype status, and reduced overall survival (OS). Kaplan-Meier and univariable Cox analyses indicated that RBM43 was related to unfavorable outcomes. Functionally, RBM43 overexpression promoted glioma cell proliferation and migration and suppressed apoptosis, whereas RBM43 knockdown exerted the opposite effects. Immune analyses revealed that elevated RBM43 expression was closely associated with macrophage M2 polarization, suggesting its involvement in immune evasion. In vivo, RBM43 overexpression accelerated tumor progression, while RBM43 knockdown inhibited tumor growth.
conclusionRBM43 is associated with glioma aggressiveness and macrophage M2-like polarization. These findings suggest that RBM43 may serve as a prognostic biomarker and a potential therapeutic target in glioma.
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