Fig. 2: Dysregulated alternative splicing events in glioma.

A Fuentes-Fayos et al. [37] uncovered the upregulation within GBM of 11 specific components of spliceosome-associated transcripts (RBM22, PRPF8, PRPF40A, TCERG1, SF3B1, SF3B1TV1, U2AF2, U2AF1, RNU5, RNU4, and RNU1), as well as the downregulation of 2 others (RNU11 and RNU12). These findings provide evidence for the implication of AS in glioma [37]. B The splicing of IG20 is regulated by the SF hnRNPH, which is elevated in gliomas [46]. By attaching to the UGGG-containing silencer at the 5’ end of exon 16, hnRNPH prevents exon 16 from being incorporated, which produces MADD, an antagonistic, anti-apoptotic isoform of IG20 [50]. This isoform reroutes TNF-a/TRAIL-induced death signaling, encouraging cell growth. C (1): El Fatimy et al. have provided evidence that miR-10b, specifically elevated in malignant gliomas, controls U6 snRNA levels, stability, conformation, and levels of N-6-adenosine methylation and pseudouridylation, as well as U6 binding to SF SART3 and PRPF8. These effects on U6 are exemplified by decreased levels of GTPase CDC42, and consequences on cell viability mediated by CDC42 [54]. D According to X. Wang, Han et al., the RBP NONO interacts with GPX1 pre-mRNA and encourages its splicing binding to its promoter, which increases the expression of GPX1 mRNA. In GBM cells, this increase of GPX1 improves antioxidant capacity and decreases oxidative stress, encouraging cell proliferation, migration, and invasion. A recent study found that the ubiquitination of NONO by TRIM25 protein, promote tumor invasion. Defective, NONO retained the second intron in PRMT1 pre-mRNA, limiting PRMT1/c-MYC pathway activation [80].“Created in BioRender. El Guendouzi, S. (2025) https://BioRender.com/g77p377”.