MicroRNA-421 promotes the proliferation and metastasis of gastric cancer cells by targeting claudin-11

Abstract

The present study aimed to evaluate the expression of microRNA (miR)-421 in gastric cancer and to investigate its biological function and underlying mechanism of action in the development of gastric cancer. The expression of miR‑421 was measured in 60 pairs of clinically removed gastric cancer tissues and matched adjacent normal gastric tissues by reverse transcription‑quantitative polymerase chain reaction. In addition, following transfection with an miR‑421 inhibitor to suppress the expression of miR‑421, the proliferation, migration and cell cycle distribution of human gastric carcinoma MKN28/MKN74 cells were determined by cell counting, Transwell and flow cytometry assays. The target gene of miR‑421 was also predicted using bioinformatic analysis and verified by dual‑luciferase reporter gene assay and western blot analysis. Furthermore, overexpression of the miR‑421 target protein was induced in MKN28/MKN74 cells to determine its function. It was observed that miR‑421 was significantly upregulated in gastric cancer tissues and that the expression of miR‑421 was associated with lymph node metastasis and the clinical stage of gastric cancer (all P<0.05). Claudin11 (CLDN11) was predicted and verified as a direct target of miR‑421. In vitro experiments demonstrated that inhibition of miR‑421 expression suppressed the proliferation and metastasis of MKN28/MKN74 cells and induced G1/S‑phase cell cycle arrest (all P<0.05). Analagous results were observed in MKN28/MKN74 cells following overexpression of the CLDN11 protein. Collectively, these data suggest that miR‑421 may promote the proliferation, invasion and metastasis of gastric cancer by inhibiting the expression of CLDN11.