Se-methylselenocysteine suppresses the growth of prostate cancer cell DU145 through connexin 43-induced apoptosis

Abstract

Se-methylselenocysteine (MSC), as a chemopreventive agent, shows antitumor effects in some cancer models, but its mechanism is still unclear. This study is to explore whether MSC induces apoptosis in prostate cancer (PCa) cells DU145 through connexin 43 (Cx43) activation. 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. 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. Student's t-test was used to calculate the difference between the groups in SPSS software. 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. As a conclusion, MSC exerts pro-apoptosis effects through increasing Cx43 expression, which in turn down-regulates Bcl-2 and up-regulates bad expression.