PURPOSE: To investigate whether Trichostatin A (TSA) possesses antitumor activity against human bladder cancer cells, and if any, its mechanism. MATERIALS AND METHODS: A human bladder cancer cell line, BIU-87, was treated with different concentrations of TSA. After treatment, cell growth was measured by MTT assay. Cell apoptosis and cell cycle changes were examined by means of flow cytometry (FCM). Apoptosis was confirmed by apoptotic ladder formation assay. mRNA expression of p21WAF1 and p53 was assessed by differential reverse transcription-polymerase chain reaction. RESULTS: Trichostatin A significantly inhibited the proliferation of bladder cancer cell at nanomolar concentrations in a time- and dose-dependent fashion. TSA treatment caused cell cycle arrest at the G1 phase and increased apoptotic cell death as shown by FCM and DNA fragmentation analysis, accompanied by increased p21WAF1 mRNA expression. In addition, TSA treatment did not alter p53 mRNA expression. CONCLUSION: Our results indicate that TSA is able to inhibit bladder cancer cell growth in vitro, possibly through p21WAF1 mediated cell cycle arrest and apoptotic cell death. This study suggests that TSA may be a potential therapeutic agent for the treatment of bladder cancer.
PURPOSE: To investigate whether Trichostatin A (TSA) possesses antitumor activity against humanbladder cancer cells, and if any, its mechanism. MATERIALS AND METHODS: A humanbladder cancer cell line, BIU-87, was treated with different concentrations of TSA. After treatment, cell growth was measured by MTT assay. Cell apoptosis and cell cycle changes were examined by means of flow cytometry (FCM). Apoptosis was confirmed by apoptotic ladder formation assay. mRNA expression of p21WAF1 and p53 was assessed by differential reverse transcription-polymerase chain reaction. RESULTS:Trichostatin A significantly inhibited the proliferation of bladder cancer cell at nanomolar concentrations in a time- and dose-dependent fashion. TSA treatment caused cell cycle arrest at the G1 phase and increased apoptotic cell death as shown by FCM and DNA fragmentation analysis, accompanied by increased p21WAF1 mRNA expression. In addition, TSA treatment did not alter p53 mRNA expression. CONCLUSION: Our results indicate that TSA is able to inhibit bladder cancer cell growth in vitro, possibly through p21WAF1 mediated cell cycle arrest and apoptotic cell death. This study suggests that TSA may be a potential therapeutic agent for the treatment of bladder cancer.
Authors: Qing Wen; Paul O'Reilly; Philip D Dunne; Mark Lawler; Sandra Van Schaeybroeck; Manuel Salto-Tellez; Peter Hamilton; Shu-Dong Zhang Journal: BMC Syst Biol Date: 2015-09-01
Authors: Michael T Buckley; Joanne Yoon; Herman Yee; Luis Chiriboga; Leonard Liebes; Gulshan Ara; Xiaozhong Qian; Dean F Bajorin; Tung-Tien Sun; Xue-Ru Wu; Iman Osman Journal: J Transl Med Date: 2007-10-12 Impact factor: 5.531
Authors: C Habold; A Poehlmann; K Bajbouj; R Hartig; K S Korkmaz; A Roessner; R Schneider-Stock Journal: J Cell Mol Med Date: 2008-04 Impact factor: 5.310