miR‑124 inhibits proliferation, migration and invasion of malignant melanoma cells via targeting versican
- Ping Yang
- Pingyuan Bu
- Chengyuan Li
- Published online on: August 22, 2017 https://doi.org/10.3892/etm.2017.4998
Copyright: © Yang
et al. This is an open access article distributed under the
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MicroRNA (miR)‑124 has been implicated in malignant melanoma (MM). However, the detailed regulatory mechanism of miR‑124 in the malignant phenotypes of MM cells has remained largely elusive. A total of 68 pairs of MM tissues and adjacent tissues were collected. Reverse‑transcription quantitative polymerase chain reaction was used to examine the mRNA expression of versican as well as the expression of miR‑124, and the protein expression of versican was assessed by western blot analysis. MTT, wound healing and Transwell assays were used to determine cell proliferation, migration and invasion, respectively. A bioinformatics analysis and a luciferase reporter assay were used to confirm the targeting association between miR‑124 and versican. miR‑124 was significantly downregulated in MM tissues compared with that in adjacent non‑tumorous tissues, and decreased expression of miR‑124 was associated with increased tumor thickness, advanced clinical stage and node metastasis of MM. Furthermore, the expression levels of miR‑124 were also reduced in MM cell lines compared with normal human skin HACAT cells. Forced overexpression of miR‑124 caused a significant reduction in the proliferation, migration and invasion of MM A375 cells. Versican was significantly upregulated in MM tissues and cell lines, and was identified as a novel target of miR‑124 in A375 cells using a luciferase reporter gene assay, and miR‑124 was revealed to negatively regulate the protein expression of versican in A375 cells. Overexpression of versican impaired the suppressive effects of miR‑124 on the proliferation, migration and invasion of A375 cells. In conclusion, miR‑124 inhibited the malignant phenotypes of MM cells at least partly via inhibition of versican. Therefore, the miR‑124/versican axis may be used as a promising therapeutic target for inhibiting MM growth and metastasis.