MiR-362-3p inhibits the proliferation, migration and EMT of gastric cancer cells by regulating the DEP-1/ERK signaling pathway.

MicroRNAs (miRNAs) play a very important role in the development of gastric cancer (GC). MiR-362-3p participates in the formation and progression of various cancers. However, the role and clinical value of miR-362-3p in GC remain unclear. The CCK8 and colony formation assays were performed to assess the effect of miR-362-3p on proliferation in GC cells. Wound healing assay and transwell assay were used to examine the migratory effects of miR-362-3p on GC cells. In silico prediction, qRT-PCR, dual luciferase reporter assays and western blot analysis were applied to confirm the target gene of miR-362-3p. The results indicated that miR-362-3p inhibited the proliferation, migration and EMT of GC cells by inhibiting the ERK signaling pathway. DEP-1 was identified to be a direct target of miR-362-3p. Knockdown of DEP-1 also suppressed the proliferation, migration and EMT of GC cells, and inhibited the ERK signaling pathway, while overexpression of DEP-1 promoted the proliferation, migration and EMT of GC cells and activated the ERK signaling pathway. miR-362-3p can suppress the proliferation, migration and EMT of GC cells through inhibiting the ERK signaling pathway by directly targeting DEP-1. Hence, miR-362-3p/DEP-1 axis may be a potential target for GC treatment.