MiR-203 inhibits tumor invasion and metastasis in gastric cancer by ATM.

Abstract

Gastric cancer is one of the most common malignancies in the world. A number of miRNAs are aberrantly expressed during the progression of gastric cancer. In this study, we aimed to investigate the role of miR-203 in the invasion and metastasis of gastric cancer and the potential mechanism of the effect of miR-203 on the tumor progression of gastric cancer. Our results showed that miR-203 was significantly downregulated in gastric cancer tissues and cells, while ataxia telangiectasia mutated kinase (ATM) was upregulated in gastric cancer tissues and cells and was directly regulated by miR-203. Ectopic overexpression of miR-203 inhibited the colony formation, migration, and invasion of gastric cancer cells. In addition, miR-203 overexpression significantly suppressed the protein level of Snail and obviously promoted the protein level of E-cadherin in gastric cancer cells. ATM knockdown phenocopied the effect of miR-203 overexpression. These results suggested that miR-203 suppressed the migration and invasion of gastric cancer through regulating the level of ATM-mediated-Snail and E-cadherin. MiR-203 might be a novel therapeutic strategy for the treatment of gastric cancer.