MicroRNA­214 promotes the EMT process in melanoma by downregulating CADM1 expression.

Melanoma is a malignant skin cancer type associated with a high mortality rate, but its treatment is currently not ideal. Both microRNA (miR)­214 and cell adhesion molecule 1 (CADM1) are differentially expressed in melanoma, but their role in this cancer type remains unknown. Therefore, the aim of the present study was to investigate the role of CADM1 and miR­214 in melanoma to identify novel targets for its treatment. The expression levels of CADM1 and miR­214 in cells were detected by reverse transcription­quantitative PCR (RT­qPCR). Moreover, cell viability, migration and invasion were measured by MTT, wound healing and Transwell assays, respectively. In addition, the relative expression levels of epithelial­mesenchymal transition (EMT)­related proteins in cells were detected by RT­qPCR and western blotting. It was found that the expression of CADM1 was inhibited in melanoma cells, while miR­214 expression was increased during melanoma tumorigenesis. Furthermore, miR­214 mimics promoted the viability, migration and invasion of melanoma cells. It was also demonstrated that the downregulation of CADM1 reversed the inhibitory effect of the miR­214 inhibitor in melanoma. Moreover, overexpression of CADM1 inhibited the EMT process in melanoma, while the miR­214 inhibitor suppressed the EMT process. The results also indicated that miR­214 promoted the EMT process by downregulating CADM1, which may represent a novel mechanism for the progression of melanoma.