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Solamargine (SM), a steroidal alkaloid glycoside purified from the Chinese traditional herb Solanum incanum , is known to possess various biological activities. However, only a few previous studies have reported the anti-metastatic activity of SM. In the present study, the inhibitory effects of SM on metastatic action were investigated in human HepG2 cells. The proliferation effects of SM on the HepG2 cells was evaluated by MTT and colony formation assays. Wound-healing and Transwell assays were performed to examine the migration and invasion effects on SM-treated HepG2 cells. The epithelial-to-mesenchymal transition (EMT)-associated markers (E-cadherin, Vimentin and N-cadherin) were detected by western blotting analysis. In the present study, MTT and colony formation assays indicated that SM suppressed HepG2 cell viability in a dose-dependent manner. The wound-healing and Transwell assays revealed that the migration and invasion activities were significantly inhibited following exposure to SM. EMT has been demonstrated to be essential for promoting migration and invasion in tumor cells and has often been characterized with a loss of epithelial markers (E-cadherin) and an increase of mesenchymal markers (Vimentin and N-cadherin). In the western blotting analysis, the expression level of E-cadherin was significantly upregulated compared with that in the control group, whereas the expression levels of N-cadherin and Vimentin were downregulated. Thus, it was suggested that the underlying mechanism of SM inhibits migration and invasion in HepG2 cells and is associated with suppression of EMT.

Solamargine inhibits the migration and invasion of HepG2 cells by blocking epithelial-to-mesenchymal transition