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MicroRNA-195 inhibits growth and invasion of laryngeal carcinoma cells by directly targeting DCUN1D1

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MicroRNAs (miRNAs) are a class of small, non-coding RNAs that regulate gene expression and are involved in cell biological processes. The aberrant expression of miR-195 has been found in various… Click to show full abstract

MicroRNAs (miRNAs) are a class of small, non-coding RNAs that regulate gene expression and are involved in cell biological processes. The aberrant expression of miR-195 has been found in various types of human cancer. However, the effect of miR-195 on the initiation and development of laryngeal squamous cell carcinoma (LSCC) remains to be elucidated. Accordingly, in the present study, we detected the expression level of miR-195 in the LSCC and the normal tissues and found that miR-195 were significantly downregulated in the LSCC tissues. Gain-of-function or loss-of-function studies including cell proliferation, wound healing assay, Transwell assay, cell cycle and apoptosis assays were performed to investigate the biological function of miR-195. Luciferase reporter assay and the rescue study confirmed that DCUN1D1 was a target of miR-195. Furthermore, DCUN1D1 expression levels were found to be upregulated in laryngeal tissues and to have a negative correlation with miR-195. We also found that both miR-195 and DCUN1D1 siRNAs can inhibit cell invasion possibly through downregulating Matrix metalloproteinase-2 (MMP-2) and Matrix metalloproteinase-9 (MMP-9) at the post-transcriptional level, which can be attenuated by restoring the expression of DCUN1D1. In summary, these data suggest that low expression of miR-195 contributes to the poor prognosis of LSCC and miR-195 regulates the proliferation and invasion ability of LSCC cells in vitro. miR-195 may suppress growth and invasion of LSCC cells possibly through targeting DCUN1D1, which would provide a candidate target for cancer therapy.

Keywords: mir 195; growth invasion; lscc; dcun1d1; expression

Journal Title: Oncology Reports
Year Published: 2017

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