microRNA-23a promotes cell growth and metastasis in gastric cancer via targeting SPRY2-mediated ERK signaling

microRNAs (miRs) serve important roles in various human cancer types. Recently, miR-23a has been indicated as an oncogene in gastric cancer, but the underlying mechanism remains unclear. In the present study, reverse transcription-quantitative polymerase chain reaction and western blot analysis was used to explore the effects of miR-23a in gastric cancer. Additionally, cell proliferation, migration and invasion were examined using an MTT assay, wound healing assay and Transwell assay, respectively. Furthermore, a luciferase reporter gene assay was used to confirm the target association. It was determined that miR-23a was significantly upregulated in gastric cancer tissues and cell lines compared with adjacent tissues, and a normal gastric epithelial cell line. Furthermore, its upregulation was significantly associated with cancer progression and poor prognosis of patients. Knockdown of miR-23a caused a notable reduction in the proliferation, migration and invasion of gastric cancer AGS cells. Sprouty homolog 2 (SPRY2) was then predicted to be target gene of miR-23a. A luciferase reporter gene assay data demonstrated that miR-23a has the ability to directly bind to the 3′-untranslational region of SPRY2 mRNA. Further investigation demonstrated that SPRY2 was significantly downregulated in gastric cancer tissues and cell lines, and the protein expression of SPRY2 was negatively regulated by miR-23a in AGS cells. Furthermore, knockdown of SPRY2 reduced the suppressive effects of miR-23a inhibition in AGS cell proliferation, migration and invasion. In addition, the activity of extracellular signal-regulated kinase (ERK) signaling was also inhibited by the miR-23a/SPRY2 knockdown in AGS cells. The present study indicated that miR-23a serves a promoting role in gastric cancer via targeting SPRY2 and downstream ERK signaling.