EIF3B is associated with m6A-related regulation of E2F7 and promotes stemness in glioblastoma multiforme

E2F transcription factors are key regulators of the cell cycle and play an important role in tumorigenesis. N6-methyladenosine (m 6 A), the most prevalent internal RNA modification in eukaryotic cells, is also crucial for cancer progression. However, the interplay between E2F family members and m 6 A modification in glioblastoma multiforme (GBM) remains poorly understood. We applied weighted gene co-expression network analysis (WGCNA) to identify m 6 A-related gene modules co-expressed with E2F7 , a gene that is significantly associated with adverse prognosis and tumor stemness. Through intersection analysis, eukaryotic translation initiation factor 3 subunit B ( EIF3B ) emerged as a hub gene, showing a strong positive correlation with E2F7 in GBM datasets. Functional validation was performed in GBM cells to assess the regulatory relationship between EIF3B and E2F7, including examination of mRNA and protein expression, mRNA stability, and m 6 A modification levels. GBM stemness was evaluated by tumor sphere formation assays and detection of stemness-associated markers. Functional validation revealed that EIF3B knockdown reduced E2F7 mRNA and protein expression, promoted E2F7 mRNA degradation, and decreased its m 6 A modification, suggesting an association between EIF3B and m 6 A-related regulation of E2F7 stability. Furthermore, EIF3B knockdown markedly suppressed GBM stemness, as demonstrated by impaired tumor sphere formation and downregulation of stemness-associated markers. Clinically, EIF3B expression increased with glioma grade and correlated with poor prognosis. Collectively, these findings suggest that the EIF3B-E2F7 axis is associated with m 6 A-related regulation in GBM and may warrant further investigation as a candidate for therapeutic targeting.