miR-124 inhibits the proliferation, migration and invasion of esophageal squamous cell carcinoma by downregulating STATS.

OBJECTIVE: To investigate the expression, role and the underlying mechanism of miR-124 in esophageal squamous cell carcinoma (ESCC). METHODS: A total of 25 pairs of ESCC and adjacent tissues were collected for analysis. The human normal esophageal epithelial cell line (Het-1A) and human esophageal cancer cell lines (EC-1) was cultured in Dulbecco's Modified Eagle Medium (DMEM) containing 10% fetal bovine serum (FBS). Cells were transfected with miR-124 mimics and inhibitors. A series of assays, including Cell-Counting-Kit-8 (CCK-8), Transwell migration and invasion assays, real-time quantitative polymerase chain reaction (RT-qPCR), enzyme-linked immunosorbent assay (ELISA) and luciferase reporter gene assay, were performed to detect the effects of miR-124 on ESCC cells. Spearman's correlation analysis was used to evaluate the relationship of miR-124 expression and signal transducer and activator of transcription-3 (STAT3) expression. RESULTS: miR-124 was significantly downregulated in ESCC tissues and cells. Overexpression of miR-124 inhibited the proliferation, migration and invasion of ESCC cells in vitro, while inhibition of miR-124 promoted these processes (all P<0.05). miR-124 was found to specifically bind to the 3'-untranslated region (3'UTR) of STAT3. The expression level of STAT3 was obviously higher in tumor tissues and cells compared to normal adjacent tissues and cells (all P<0.05). Moreover, miR-124 expression was negatively associated with STAT3 levels. Restoring STAT3 expression in ESCC cells transfected with miR-124 mimics partially reversed the inhibitory effects of miR-124 mimics on cell proliferation, migration, and invasion. Conversely, inhibiting STAT3 expression in ESCC cells transfected with miR-124 inhibitors partially abolished the promoting effects of miR-124 inhibitors on the proliferation, migration and invasion of ESCC cells. CONCLUSION: miR-124 inhibits the proliferation, migration and invasion of ESCC cells by downregulating STATS, indicating that miR-124 may serve as a molecular candidate for treating ESCC.