Effects of miR-106b-3p on cell proliferation and epithelial-mesenchymal transition, and targeting of ZNRF3 in esophageal squamous cell carcinoma

Previous studies have demonstrated that the dysregulation of microRNAs (miRs) is frequently associated with cancer progression. Deregulation of miR-106b-3p has been observed in various types of human cancer. However, the biological function of miR-106b-3p in esophageal squamous cell carcinoma (ESCC) remains unclear. Thus, the aim of this study was to investigate the role of miR-106b-3p in ESCC. In the current study, the results indicated that miR-106b-3p was upregulated in ESCC cell lines and tissues. An increase in miR-106b-3p using miR mimics significantly promoted the proliferation of ESCC cells in vitro. Furthermore, the results demonstrated that miR-106b-3p overexpression promoted migration, invasion and epithelial-mesenchymal transition (EMT) of ESCC cells. In addition, zinc and ring finger 3 (ZNRF3) was identified as a target of miR-106b-3p in ESCC cells, and the ZNRF3 expression level was inversely associated with miR-106b-3p. It was also demonstrated that miR-106b-3p has a role in EMT by regulating Wnt/β-catenin signaling pathway in ESCC. In conclusion, these data suggested that miR-106b-3p promotes cell proliferation and invasion, partially by downregulating ZNRF3 and inducing EMT via Wnt/β-catenin signaling in ESCC cells. Thus, miR-106b-3p and ZNRF3 may be novel molecular targets for the future treatment of ESCC.