siRNA Targeting of the <b><i>SNCG</i></b> Gene Inhibits the Growth of Gastric Carcinoma SGC7901 Cells in vitro and in vivo<b> </b>by Downregulating the Phosphorylation of AKT/ERK

The aim of the study was to evaluate the effects of synuclein-&#x03B3; (<i>SNCG</i>) silencing on gastric cancer SGC7901 cells and to elucidate the associated mechanisms. pGCSIL-lentiviral siRNA targeting of the <i>SNCG</i> gene was employed to inhibit <i>SNCG</i> expression. Several experiments such as quantitative real-time PCR, Western blotting, MTT, colony formation, migration assay, and flow cytometry were performed to investigate the biological behavior of infected SGC7901 cells. BALB/c nude mice were used as tumor xenograft models to assess the effects of <i>SNCG</i> silencing on tumor growth. Western blot analysis was carried out to determine the relative levels of AKT, p-AKT, ERK, and p-ERK expression. Our results showed that <i>SNCG </i>was overexpressed in SGC7901 cells as compared to normal gastric mucosal epithelial cells. SGC7901 cells transfected with <i>SNCG</i> siRNA demonstrated significantly decreased gastric cancer growth (<i>p</i> < 0.01), reduced cell migration, cell cycle arrest in the G0/G1 phase, promoted tumor cell apoptosis (<i>p</i> < 0.01), and inhibited tumorigenesis in xenograft animal models. Western blot analysis indicated that the protein levels of p-AKT and p-ERK were much lower in the <i>SNCG</i> siRNA group than in the control groups. The results of the present study suggest that <i>SNCG</i> siRNA plays a significant role in the proliferation, migration, and tumorigenesis of gastric cancer by downregulating the phosphorylation of AKT and ERK. RNA interference-mediated silencing of <i>SNCG</i> may provide an opportunity to develop a novel treatment strategy for gastric cancer.