UCHL5 promotes Tumorigenesis of Bladder Cancer by Activating AKT/mTOR signaling pathway and targeting c-myc, SLC25A19, and ICAM5.

Purpose: To investigate the tumor-promoting role of UCHL5 in bladder cancer. Method: We established the UCHL5 knockdown cell line in which the target gene was knocked down by shRNA. RNA was extracted from cells using trizol reagent(Invitrogen) Result: Through RNA-sequencing analysis of wild-type and UCHL5 deficient T24 cell lines, the downstream signaling pathways that UCHL5 may be involved in were determined. We found that the AKT/mTOR signaling pathway and c-Myc,SLC25A19, and ICAM5 were significantly inactivated when UCHL5 was knocked down in bladder cancer. Conclusion: UCHL5 enhances the AKT/mTOR pathway, which consequently upgraded the expression of c-myc,SLC25A19, and ICAM5, ultimately promoting the occurrence and progression of bladder cancer. UCHL5 may suggest potential utility for bladder cancer therapy. Comparative gene expression profiling analysis of RNA-seq data for T24 cells and its KD derivatives (shUCHL5).