CONTEXT - Se-methylselenocysteine (MSC), as a chemopreventive agent, shows antitumor effects in some cancer models, but its mechanism is still unclear.
AIMS - This study is to explore whether MSC induces apoptosis in prostate cancer (PCa) cells DU145 through connexin 43 (Cx43) activation.
SETTINGS AND DESIGN - The experiment was performed in a PCa cell line model DU145 and using a series of biological assay methods to investigate the regulating pathway from MSC through Cx43 to downstream molecules, demonstrating an important role of Cx43 in PCa development and as a potential treatment target.
MATERIALS AND METHODS - The human PCa cell line DU145 was used as a model. The effects of MSC on Cx43 expression were examined by reverse transcription-polymerase chain reaction, western blot; effects on cell growth and proliferation were determined by WST-1 and colony formation assay; small interfering ribonucleic acid was used to evaluate the direct contribution of Cx43 to cancer cell apoptosis.
STATISTICAL ANALYSIS USED -Student's t-test was used to calculate the difference between the groups in SPSS software.
RESULTS - Results showed that MSC inhibited the growth and colony formation of the DU145 cells; MSC induced cell apoptosis by increasing Cx43 expression at messenger ribonucleic acid and protein levels; MSC decreased B-cell lymphoma-2 (Bcl-2) and increased bad levels of DU145 cells.
CONCLUSIONS - As a conclusion, MSC exerts pro-apoptosis effects through increasing Cx43 expression, which in turn down-regulates Bcl-2 and up-regulates bad expression.
Journal of cancer research and therapeutics. 0000 [Epub]
Zhong Lu, Li Qi, Gui-Xin Li, Xue-Jun Bo, Guo-Dong Liu, Jun-Ming Wang
Department of Oncology, Clinical College of Weifang Medical University, Weifang 261031, China.