Mir-200c Regulates The Proliferation, Apoptosis And Invasion Of Gastric Carcinoma Cells Through The Downregulation Of Ednra Expression

This study aimed to investigate the regulatory effects of microRNA (miR)-200c on the proliferation, apoptosis and invasion of gastric carcinoma cells and to elucidate the underlying mechanisms involving the possible role of endothelin receptor A (EDNRA). The expression levels of miR-200c and EDNRA in the gastric carcinoma cell lines, BGC-823, SGC-7901 and HGC-27, and in GES-1 normal gastric cells were evaluated by RT-PCR and western blot analysis. The gastric carcinoma cells, particularly the BGC-823 cells, expressed significantly lower levels of miR-200c than the normal gastric cells (P<0.01). Thus, the BGC-823 cells were employed as model cells. In comparison to the normal gastric cells, EDNRA was overexpressed in the gastric carcinoma cells (P<0.01). Following the transfection of the gastric carcinoma cells with miR-200c mimics, or negative control vector (miR-200c NC), or with siRNA targeting EDNRA (siRNA EDNRA) or negatvie control siRNA (siRNA NC), the expression levels were assessed again by RT-PCR and western blot analysis. The successful transfection of miR-200c mimics was observed and this markedly elevated the expression of miR-200c (P<0.01). The transfection of miR-200c mimics or siRNA EDNRA notably decreased the EDNRA mRNA and protein expression levels (both P<0.01). In additoin, dual-luciferase reporter gene analysis was performed to reveal the targeting relationship between miR-200c and EDNRA. EDNRA was found to be the downstream target gene of miR-200c. Moreover, methyl thiazolyl tetrazolium (MTT) assay, Hoechst staining and Transwell assay were conducted to demonstrate the effects of miR-200c mimics or siRNA EDNRA on the proliferation, apoptosis and invasion of the gastric carcinoma cells, respectively. We found that transfection with miR-200c mimics and siRNA EDNRA were able to markedly suppress the proliferation and invasive capacity, and to promote the apoptosis of the gastric carcinoma cells (all P<0.01). On the whole, our data indicate that miR-200c regulates the proliferation, apoptosis and invasion of gastric carcinoma cells through the downregulation of EDNRA expression.