MicroRNA3650 Promotes Gastric Cancer Proliferation and Migration through the PTEN/PI3K-AKT-mTOR and Hippo Pathways.

Abstract

Gastric cancer (GC) is a malignant tumor with seriously poor outcomes. Studies have shown that microRNAs (miRNAs) play an omnifarious regulatory effect in GC. However, the role of miR-3650 in the progression of GC is not well known. In this study, miR-3650 expression and its clinical significance were determined using clinical specimens. The biological functions of miR-3650 were determined in gastric cancer cell lines through CCK-8, cell scratch, and transwell experiments. Bioinformatics predictions, combined with Western blot experiments, were employed to explore its downstream molecular targets. We observed that miR-3650 was overexpressed in GC specimens and most cell lines, i.e., 77.8% (MKN28, SNU1, AGS, MKN45, N87, BGC823 and SGC7901). The overexpression correlated with advanced T-stage, N-stage, M-stage, and TNM-stage. Furthermore, miR-3650 promoted the proliferation and migration of gastric cancer cells, and its overexpression promoted the PI3K-AKT-mTOR pathway and inhibited the PTEN and hippo pathways. The potassium ion signaling pathway was also involved in the biological process of miR-3650 promoting cancer. Therefore, we concluded that miR-3650/PTEN/PI3K-AKT-mTOR and miR-3650/hippo pathways are vital in the progression of GC and serve as novel targets for GC therapy.