ArticleDiscover oncology2026
RBM15B enhancing ITGA1 mRNA stability can accelerate glioblastoma tumorigenesis via the PI3K-Akt pathway.
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
backgroundN6-methyladenosine (m6A) modification is a key regulatory mechanism involved in the tumorigenesis of glioblastoma (GBM). The oncogenic role of m6A writer RNA-binding motif protein 15B (RBM15B) has been confirmed in multiple cancers. However, its role and regulatory mechanism in GBM remain unclear. This study aimed to explore the role of RBM15B interacting with integrin alpha-1 (ITGA1) in GBM.
methodsGEPIA, GEO DataSets and CGGA database were investigated to confirm the levels of RBM15B and the correlation between RBM15B and ITGA1 in GBM. Quantitative reverse transcription polymerase chain reaction (qRT-PCR) was performed to further verify RBM15B and ITGA1 levels in GBM samples. The effects of RBM15B and ITGA1 on GBM cells were determined through cell functional experiments and an animal assay. The interaction between RBM15B and ITGA1 was detected using qRT-PCR, methylated RNA immunoprecipitation assay, and actinomycin D therapy. The effects of RBM15B and ITGA1 on phosphoinositide 3-kinase–protein kinase B (PI3K–Akt) pathway-related proteins were assessed by Western blotting.
resultsRBM15B was highly expressed in GBM, and RBM15B downregulation suppressed GBM cell proliferation, migration, invasion, and tumor growth. ITGA1 mRNA stability decreased by reducing its m6A modification level by downregulating RBM15B. Furthermore, ITGA1 overexpression induced GBM cell malignancy by activating the PI3K–Akt pathway; however, downregulating RBM15B partly reversed the effects of ITGA1 overexpression.
conclusionThis study uncovers a novel mechanism by which RBM15B promotes ITGA1 mRNA stability through m6A modification, leading to the activation of the PI3K–Akt pathway and promoting GBM progression.
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