Effect of total saponins of Schizocapsa plantaginea Hance on epithelial mesenchymal transformation, migration and invasion of WB-F344 malignant transformed cells

Objective: To investigate the effect and mechanism of total saponins of Schizocapsa plantaginea Hance (SSPHs) on epithelial mesenchymal transformation (EMT), migration and invasion of WB-F344 malignant transformed cells. Methods: A malignant transformation cell model was prepared by inducing rat hepatic oval cell line WB-F344 in vitro using the carcinogenic agent 1-methyl-3-nitro-1-nitrosoguanidine (MNNG). The experiment was divided into control group, MNNG group, MNNG+SSPHs group, MNNG+Wnt-1/β-catenin signaling pathway activator lithium chloride (LiCl)+signaling pathway inhibitor (XAV-939) group, MNNG+LiCl group, and MNNG+LiCl+SSPHs group. Cell counting kit-8 (CCK-8) assay was used to detect the activity of SSPHs on WB-F344 malignant transformed cells; cell scratch assay and Transwell assay were used to detect the migration and invasion ability of WB-F344 malignant transformed cells, respectively. The expression of E-cadherin, N-cadherin, Vimentin, Wnt-1 and β-catenin proteins was detected by western blotting. Results: After SSPHs treatment, the activity of malignant transformed cells of WB-F344 was inhibited (P＜0.05). Compared with the control group, the MNNG group showed an increased scratch healing rate, an increased number of cell membrane penetration, elevated expression levels of N-cadherin, Vimentin, Wnt-1, β-catenin proteins, and a decreased expression level of E-cadherin protein (all P＜0.05). Compared with the MNNG group, the MNNG + SSPHs group showed a decrease in scratch healing rate, a decrease number of membrane penetration, down-regulation of N-cadherin, Vimentin, Wnt-1 and β-catenin protein expression, and up-regulation of E-cadherin protein expression (all P＜0.05). Compared with the MNNG+LiCl group, the protein expression of N-cadherin, Vimentin, Wnt-1 and β-catenin in the MNNG+LiCl+SSPHs group was down-regulated, while the protein expression of E-cadherin was up-regulated (all P＜0.05), and the results were the same as those of MNNG+LiCl+XAV-939 group. Conclusion: SSPHs can inhibit EMT, migration and invasion of WB-F344 malignant transformed cells, and the mechanism may be related to the regulation of Wnt-1/β-catenin signaling pathway.