MicroRNA 495 Inhibits Proliferation and Metastasis and Promotes Apoptosis by Targeting Twist1 in Gastric Cancer Cells

Abstract

Recently, microRNAs (miRNAs) have reported to participate in multiple biological processes. However, the effects of miR-495 on gastric cancer (GC) remain unclear. The purpose of this study is to explore the functions of miR-495 in GC cells proliferation, metastasis and apoptosis. SGC-7901 and BGC-823 were transfected with miR-495 mimic, miR-495 inhibitor and negative controls (mimic control and inhibitor control). The expressions of miR-495, cell viability, migration, apoptosis and apoptosis-related factors were examined by qRT-PCR, trypan blue staining, Transwell, flow cytometry and western blot, respectively. Simultaneously, the key factors expressions of EMT were detected by qRT-PCR again. The direct target gene of miR-495 was confirmed by dual luciferase assay. Additionally, sh-Twist1, pc-Twist1 and corresponding control were also transfected into SGC-7901 and BGC-823 cells, and then the protein levels of EMT-associated factors were detected by western blot. MiR-495 was down-regulated in GC cells. MiR-495 expression level was effectively overexpressed or suppressed in SGC-7901 and BGC-823 cells. Overexpression of miR-495 significantly decreased cell viability, migration and increased apoptosis as well as inhibited EMT process. Suppression of miR-495 showed contrary results. Twist1 was clarified as a target gene of miR-495, and Twist1 silencing obviously reduced the promotion effect of miR-495 suppression on these biological processes. Besides, Twist1 silencing significantly blocked EMT signal pathway in both SGC-7901 and BGC-823 cells. MiR-495 inhibited proliferation, metastasis and promoted apoptosis by targeting Twist1 in GC cells. These data indicated that miR-495 might be a novel anti-tumor factor of GC and provide a new method for treatment of GC.

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Competing Endogenous RNA Networks in the Epithelial to Mesenchymal Transition in Diffuse-Type of Gastric Cancer

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