Lobaplatin arrests cell cycle progression, induces apoptosis and impairs migration and invasion in B16-F10 melanoma cell line in vitro

Melanoma is highly resistant to most conventional treatment, and the incidence and mortality rates are increasing rapidly worldwide. The objective of this study was to determine the anticancer effects of lobaplatin on the melanoma carcinoma cell line B16-F10 in vitro, and explored its mechanisms of action. Our results have shown that lobaplatin inhibited cell proliferation in human melanoma A375 and CHL-1 cells and murine melanoma B16-F10 cells in a concentration- and time-dependent manner. Flow cytometry assay confirmed that lobaplatin affected B16-F10 cell survival by blocking cell cycle progression in G2/M phase and inducing apoptosis in a concentration-dependent manner. In addition, the apoptosis was associated with downregulation of anti-apoptotic protein Bcl-2 while upregulation of pro-apoptotic protein Bax. Lobaplatin could also decrease the mitochondrial membrane potential, indicating that lobaplatin may induce apoptosis via mitochondria-mediated apoptotic pathway. Furthermore, lobaplatin blocked B16-F10 cell migration and invasion in vitro. These results suggested that lobaplatin could be an effective chemotherapeutic agent in melanoma treatment by inhibiting proliferation, inducing apoptosis, cell cycle arrest and blocking cell migration and invasion.