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2017 ; 51
(1
): 158-168
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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
): 158-168
PMID28534939
show 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 downregulation 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.