Feng Jiang,1 Pengfei Wu2 1Department of Urology, Shanghai Pudong New Area People’s Hospital, Shanghai 201200, People’s Republic of China; 2Department of Urology, Tenth People’s Hospital of Tongji University, Shanghai 200072, People’s Republic of ChinaCorrespondence: Pengfei WuDepartment of Urology, Tenth People’s Hospital of Tongji University, 301 Yanchang Road, Jing’an District, Shanghai 200072, People’s Republic of ChinaEmail wupengfei900@126.comBackground: Prostate cancer threatens the life and health of men in China. Desmocollin-2 (DSC2) is a member of DSC family, abnormal expression of which can affect the invasion and metastasis of tumor cells. The aim of this study was to investigate the role of DSC2 in prostate cancer.Materials and Methods: Regulating DSC2 expression in prostate cancer cells was conducted with transfection. The expression of DSC2, apoptosis-related proteins, cell cycle-related proteins and E-cadherin (E-cad)/β-catenin pathway was detected by Western blot analysis. The proliferation, clone formation ability, migration, invasion and apoptosis of transfected cells were in turn detected by cell counting kit-8 (CCK-8) assay, clone formation assay, wound healing assay, transwell assay and flow cytometry analysis.Results: DSC2 expression was increased in prostate cancer cells compared with RWPE-1 cells. Inhibition of DSC2 promoted the proliferation, clone formation ability, migration and invasion while suppressed apoptosis of LNCaP cells and PC-3 cells. Inhibition of DSC2 affected the expression of apoptosis-related proteins and cell cycle-related proteins according to the changes of apoptosis and proliferation. Furthermore, inhibition of DSC2 up-regulated the expression of p-β-catenin and EGFR while down-regulated the expression of E-cad. DSC2 overexpression exerted the opposite effect of inhibition of DSC2 on LNCaP cells and PC-3 cells.Conclusion: DSC2 expression was increased in prostate cancer cells. In addition, inhibition of DSC2 promoted the proliferation, clone formation ability, migration and invasion while suppressed apoptosis of LNCaP cells and PC-3 cells, which provided the fundamental basis for treatment of prostate cancer.Keywords: DSC2, proliferation, apoptosis, prostate cancer cell
