Research Paper Volume 16, Issue 8 pp 6757—6772
USP15 facilitates the progression of bladder cancer by amplifying the activation of the NF-κB signaling pathway
Figure 8. USP15 stabilizes BRCC3 through deubiquitination. (A) Co-IP between endogenous BRCC3 and USP15 in J82 cells. (B) J82 cells were treated with 15 μM proteasomal inhibitor MG132 for the indicated time, and the protein levels of BRCC3 were then detected. (C) J82 cells transfected with USP15 shRNA were treated with MG132 (15 μM). Cells were collected at 6 h and immunoblotted with the antibodies indicated. (D) J82 cells were transfected with or without p-USP15, and treated with cycloheximide (CHX). Cells were collected at different time points and immunoblotted with the antibodies indicated. (E) Quantitative results of relative BRCC3 protein levels in D (**p < 0.01). (F) The knockdown or exogenous expression of USP15 altered the ubiquitination of BRCC3 in J82 cells treated with MG132 (15 μM). The levels of ubiquitin-attached BRCC3 were detected by Western blotting analysis with Ub antibody.