microRNA-425-5p is upregulated in human gastric cancer and contributes to invasion and metastasis in vitro and in vivo.

Emerging evidence indicates that microRNAs are involved in the development and progression of gastric cancer (GC), functioning as tumor suppressors or oncogenes. The aim of the current study was to explore the potential mechanism of microRNA-425-5p (miR-425-5p) in GC. Using reverse transcription quantitative polymerase chain reaction, miR-425-5p expression was detected in GC cell lines (SGC-7901, MKN-28, MKN-45, BGC-823 and AGS) and the GES-1 cell line. Cell proliferation, soft agar colony formation, flow cytometry, haptotactic migration and matrigel chemoinvasion assays were used to test the proliferation, apoptosis, invasion and migration of BGC-823 cells transfected with miR-425-5p mimics or an inhibitor. Female BALB/c mice were randomly divided into three groups. Each experimental group contained five mice. BGC 823 cells were stably transfected with miR-425-5p inhibitor, wild type or negative control and were injected into the mice through the tail vein. It was found that miR-425-5p expression was significantly upregulated in all the GC cell lines when compared with the GES-1 cell line. Downregulation of miR-425-5p expression inhibited GC cell proliferation, invasion and migration. In the in vivo studies, downregulation of miR-425-5p expression suppressed pulmonary metastasis in the nude mice. Thus, miR-425-5p was demonstrated to have the potential to become a novel metastasis-associated gene; however, the mechanisms associated with these effects require further study. In the future, the development of miR-425-5p as a novel therapeutic strategy for the treatment of GC may be possible.