miR-181a modulates proliferation, migration and autophagy in AGS gastric cancer cells and downregulates MTMR3.

MicroRNAs (miRs) have emerged as crucial regulators of tumorigenesis by regulating post-transcriptional gene expression. miR-181a was previously demonstrated to be overexpressed in human gastric cancer tissues and cell lines, whereas MTMR3 was underexpressed. The MTMR3 gene was identified as a direct target of miR-181a. However, its functional role in gastric cancer remains to be established. In the present study, miR‑181a was demonstrated to inhibit MTMR3 expression in AGS cells. Ectopic expression of miR‑181a mimics or introduction of MTMR3 small interfering RNA resulted in an increase in cell proliferation, colony formation, migration, invasion, as well as suppression of apoptosis. Further investigation in the present study indicated that overexpression of miR‑181a, or depletion of MTMR3, attenuated starvation‑induced autophagy in AGS cells. In addition, inhibition of endogenous miR‑181a led to stimulation of autophagic activity. Collectively, these data suggest that miR‑181a is a novel regulator of gastric cancer progression and autophagy, and miR-181a modulation may be a potential strategy for the development of miRNA‑based therapeutics for gastric cancer.