期刊
MOLECULAR MEDICINE REPORTS
卷 13, 期 4, 页码 3349-3355出版社
SPANDIDOS PUBL LTD
DOI: 10.3892/mmr.2016.4901
关键词
non-small cell lung cancer; microRNA; zinc finger E-box-binding homeobox 2; metastasis; epithelial-mesenchymal transition
MicroRNAs (miRs) have been demonstrated to regulate various biological processes in human cancer, including non-small cell lung cancer (NSCLC). However, little evidence has been provided regarding the exact role of miR-200c in mediating the malignant progression of NSCLC, as well as the underlying mechanism. The present study aimed to investigate the putative role of miR-200c in the progression of NSCLC. The expression levels of miR-200c were significantly reduced in NSCLC cell lines compared with in normal lung epithelial cells, as determined by reverse transcription-quantitative polymerase chain reaction. Overexpression of miR-200c significantly suppressed cell migration and invasion of A549 NSCLC cells. Results of a luciferase reporter assay further identified zinc finger E-box-binding homeobox 2 (ZEB2) as a direct target gene of miR-200c, and the expression of ZEB2 was shown to be suppressed in A549 cells overexpressing miR-200c. Furthermore, small interfering RNA-mediated inhibition of ZEB2 suppressed the migration and invasion of A549 cells. In addition, since ZEB2 is an epithelial-mesenchymal transition (EMT) regulator, the role of miR-200c in the regulation of EMT in NSCLC cells was further examined. Results of a western blot analysis indicated that overexpression of miR-200c upregulated E-cadherin, and downregulated N-cadherin and vimentin expression in A549 cells, thus suggesting that EMT was suppressed. Based on these results, the present study suggested that miR-200c was able to inhibit the metastasis of NSCLC cells by targeting ZEB2. Therefore, miR-200c may be considered as a potential candidate for the treatment of NSCLC.
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