Ginsenoside Rg3 to regulate the EMT induced by TGF-in gastric cancer.

Abstract

e23200 Background: To discuss the regulate effect of Ginsenoside Rg3 during the TGF-β1 induced EMT in human gastric cancer SNU-601 cell line. Methods: In the first part of our experiment, ninety-nine patients who were diagnosed as gastric cancer were admitted to this study eventually. The Luminex® xMAP technology was used to measure the plasma levels of TGF-β1. In the second part, human gastric cancer SNU-601 cell line were cultured normally. Inverted microscope was used to observe morphological changes. The cell relative growth rate of proliferation was analyzed by MTT assay. Wound-healing assay and transwell invasion assay were carried out to predict the capacity of Ginsenoside Rg3 in inhibiting migration and invasion. Western Blot was performed to analyze the influence of Ginsenoside Rg3 and TGF-β1 on the protein expression of E-cadherin and Vimentin. Results: The plasma cytokine levels of TGF-β1 were associated with vessel invasion, peritoneal involvement, TNM stage, T stage, N stage in gastric cancer patients. In Vitro Study, TGF-β1 stimulated epithelial-mesenchymal transition in SNU-601 cell lines. Ginsenoside Rg3 inhibited the TGF-β1 induced morphological changes, cell proliferation increase, cell migration and cell invasion. Ginsenoside Rg3 markedly increased expression of the epithelial marker E-cadherin, and repressed the upregulation and expression of the mesenchymal marker Vimentin during the TGF-β1 induced EMT in SNU-601 cell line. Conclusions: The plasma cytokine levels of TGF-β1 were associated with vessel invasion, peritoneal involvement, tumor stage in gastric cancer patients. TGF-β1 stimulated biological malignant behavior through EMT in gastric cancer. Ginsenoside Rg3 could inhibit the EMT induced by TGF-β1 in SNU-601 cell lines.