Upregulation of microRNA-27b contributes to the migration and invasion of gastric cancer cells via the inhibition of sprouty2-mediated ERK signaling

MicroRNAs (miRs) have been demonstrated to be associated with the development, progression and prognosis of gastric cancer. However, the exact role of miR-27b in the regulation of gastric cancer cells and the underlying mechanisms remain unclear. In the current study, it was demonstrated that miR-27b was significantly upregulated in gastric cancer tissues and cell lines, compared with their matched normal adjacent tissues and normal gastric epithelial cells, respectively. Luciferase reporter assay data indicated that sprouty2 (SPRY2) is a direct target of miR-27b, and miR-27b binds to the 3′-untranslated region of SPRY2 mRNA. Overexpression of miR-27b led to a significant reduction in the protein expression of SPRY2, while knockdown of miR-27b enhanced the SPRY2 protein expression in gastric cancer cells. Furthermore, knockdown of miR-27b promoted migration and invasion in gastric cancer cells, exhibiting similar effects to those of SPRY2 overexpression on the migration and invasion of gastric cancer cells. Investigation of the molecular mechanisms identified that the activity of extracellular signal-related kinase (ERK) signaling was mediated by miR-27b and SPRY2 in gastric cancer cells. In addition, it was observed that SPRY2 was frequently downregulated in gastric cancer tissues compared with their matched normal adjacent tissues. In summary, it was suggested that miR-27b promotes the migration and invasion of gastric cancer cells via inhibition of SPRY2-mediated ERK signaling. Therefore, miR-27b/SPRY2 may be used as a potential target for the treatment of gastric cancer.