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Deprecated: Implicit conversion from float 284.79999999999995 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Int+J+Oncol 2017 ; 51 (1): 158-68 Nephropedia Template TP
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miR-181b-5p mediates TGF-?1-induced epithelial-to-mesenchymal transition in non-small cell lung cancer stem-like cells derived from lung adenocarcinoma A549 cells #MMPMID28534939
Li X; Han J; Zhu H; Peng L; Chen Z
Int J Oncol 2017[Jul]; 51 (1): 158-68 PMID28534939show ga
The ability of non-small cell lung cancer (NSCLC) cells to invade and metastasize is associated with epithelial-to-mesenchymal transition (EMT). The process of EMT is, at least in part, regulated by microRNAs. However, it is unknown whether microRNAs regulate EMT in cancer stem-like cells (CSLCs), or which microRNAs are involved. In the present study, we compared microRNA expression in A549 cells, TGF-?1-treated A549 cells, CSLCs characterized by the CD133+/CD326+ phenotype, and TGF-?1-treated CSLCs. We found that miR-181b-5p expression was upregulated by TGF-?1. Moreover, the overexpression of the miR-181b-5p in A549 cells and CD133+/CD326+ cells resulted in the down-regulation of the E-cadherin and increased invasion and metastasis in vitro and in vivo. Accordingly, the knockdown of miR-181b-5p partially restored E-cadherin expression. These results suggest that miR-181b-5p regulates TGF-?1-induced EMT by targeting E-cadherin not only in normal A549 cells but also in CD133+/CD326+ cells which have characteristics of CSLCs. Thus, miR-181b-5p represents a new therapeutic target in NSCLC.