MicroRNA‑214 promotes the EMT process in melanoma by downregulating CADM1 expression
- Shu‑Jun Wang
- Wei‑Wei Li
- Cong‑Ji Wen
- Yong‑Li Diao
- Tian‑Lan Zhao
Affiliations: Department of Plastic Surgery, The Second Affiliated Hospital of Soochow University, Suzhou, Jiangsu 215004, P.R. China, Department of Burns and Plastic Surgery, Yancheng City No.1 People's Hospital, Yancheng, Jiangsu 224005, P.R. China
- Published online on: August 20, 2020 https://doi.org/10.3892/mmr.2020.11446
Copyright: © Wang
et al. This is an open access article distributed under the
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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 miR‑214 in melanoma to identify novel targets for its treatment. The expression levels of CADM1 and miR‑214 in cells were detected by reverse transcription‑quantitative PCR (RT‑qPCR). Moreover, cell viability, migration and invasion were measured by MTT, wound healing and Transwell assays, respectively. In addition, the relative expression levels of epithelial‑mesenchymal transition (EMT)‑related proteins in cells were detected by RT‑qPCR and western blotting. It was found that the expression of CADM1 was inhibited in melanoma cells, while miR‑214 expression was increased during melanoma tumorigenesis. Furthermore, miR‑214 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 miR‑214 inhibitor in melanoma. Moreover, overexpression of CADM1 inhibited the EMT process in melanoma, while the miR‑214 inhibitor suppressed the EMT process. The results also indicated that miR‑214 promoted the EMT process by downregulating CADM1, which may represent a novel mechanism for the progression of melanoma.