Knockdown of ubiquitin associated protein 2-like inhibits the growth and migration of prostate cancer cells

Abstract

The ubiquitin-proteasome system (UPS) is involved in the development of cancer in various functions. Inhibition of the ubiquitin-proteasome has been revealed to be a powerful therapeutic method for carcinoma. Ubiquitin associated protein 2-like (UBAP2L) is believed to be involved in the ubiquitin-proteasome pathway; however, the role of UBAP2L in human prostate cancer is still unknown. In the present study, we found that UBAP2L was expressed in a number of prostate carcinoma cell lines. Using lentiviral-mediated RNA interference (RNAi), we efficiently knocked down endogenous UBAP2L expression at the mRNA and protein levels. After UBAP2L disruption, the proliferation and colony formation ability were significantly reduced in the PC-3 and DU145 cells. Flow cytometric analysis showed that UBAP2L knockdown blocked cell cycle progression. Downregulation of UBAP2L inhibited the migration of PC-3 and DU145 cells, as determined by Transwell assay. Moreover, depletion of UBAP2L blocked the AMPKα, Bad and PRAS40 signaling pathways. In conclusion, our results suggest that UBAP2L may play a role in prostate cancer growth and metastasis, and knockdown of UBAP2L by RNAi may serve as a potential therapeutic approach for prostate cancer.