Fig. 7

Schematic model illustrating the role of TRIM25 in glioblastoma cell growth and invasion. TRIM25 mediates the K63-linked ubiquitination of NONO and maintains normal physiological functions of NONO in GBM cells. TRIM25 knockdown reduces the K63-linked ubiquitination of NONO, which inhibits the splicing function of NONO. The dysfunctional NONO further leads to the retention of the second intron in the pre-mRNA of PRMT1 and suppresses the production of mature PRMT1 mRNA, thereby inhibiting the activation of the c-MYC pathway