Terazosin Suppress Human Prostatic Cancer PC3 Cell Viability via Proteasome InhibitionShujue Li#, Wenzheng Wu#, Weidong Ji#, Yeping Liang#, Lili Ou#, Guohua Zeng*, and Wenqi Wu
Department of Urology, Minimally Invasive Surgery Center, The First Affiliated Hospital of Guangdong Key Laboratory of Urology, Guangzhou medical University,Guangdong, 510230, China
- *Corresponding Author:
- Guohua Zeng
Wenqi Wu, Department of Urology
Minimally Invasive Surgery Center
The First Affiliated Hospital of Guangdong Key Laboratory of Urology
Guangzhou Medical University
E-mail: [email protected]; [email protected]
Received Date: May 22, 2014; Accepted Date: June 12, 2014; Published Date: June 19, 2014
Citation: Shujue Li#, Wenzheng Wu#, Weidong Ji#, Yeping Liang#, Lili Ou#, Guohua Zeng*, Wenqi Wu* (2014) Terazosin Suppress Human Prostatic Cancer PC3 Cell Viability via Proteasome Inhibition. Biol Med 6:203. doi: 10.4172/0974-8369.1000203
Copyright: © 2014 Zeng, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution and reproduction in any medium, provided the original author and source are credited.
Terazosin is one of classic quinazoline-based selective α1-adrenoreceptor antagonists, which is usually used for the treatment of benign prostate hyperplasia (BPH) patients. Several evidences suggest that terazosin can induce apoptosis of prostatic cancer cells in vitro and suppress prostatic tumor growth in vivo, but molecular mechanism contributing to these processes has not yet been fully elucidated. In this study, we report that the suppression of terazosin on prostatic cancer PC3 cells viability partially mediated by proteasome inhibition. We first examined cytotoxicity of terazosin in human prostatic cancer cell line PC3, including cell viability, cell cycle analysis and cell apoptosis analysis. Then the chymotrypsin-like proteasome activity, levels of ubiquitinated-proteins and selective protein substrate of proteasome were detected, to reflect alteration of proteasome activity. Our results indicate that terazosin treatment results in a significant decrease of cell viability in a dose- and time- dependent manner in PC3 cells, accompanied with cell cycle arrest and apoptotic induction; Exposure to terazosin also causes a significant loss of proteasome activity as well as accumulation of ubiquitinated-proteins and selective protein substrate P27 in PC3 cells, which occurs prior to cell death. In view of these results, we conclude that terazosin suppress human prostatic cancer PC3 cell viability by cell cycle arrest and cell death induction, which is associated with its proteasome inhibitory activity.