@Article{096504019X15565325878380,
AUTHOR = {Ming Zhang, Baochang Shi, Kai Zhang},
TITLE = {miR-186 Suppresses the Progression of Cholangiocarcinoma Cells  Through Inhibition of Twist1},
JOURNAL = {Oncology Research},
VOLUME = {27},
YEAR = {2019},
NUMBER = {9},
PAGES = {1061--1068},
URL = {http://www.techscience.com/or/v27n9/48635},
ISSN = {1555-3906},
ABSTRACT = {Deregulation of miR-186 and Twist1 has been identified to be involved in the progression of multiple cancers. 
However, the detailed molecular mechanisms underlying miR-186-involved cholangiocarcinoma (CCA) are 
still unknown. In this study, we found that miR-186 was downregulated in CCA tissues and cell lines, and 
negatively correlated with the expression of Twist1 protein. In vitro assays demonstrated that miR-186 mimics repressed cell proliferation, in vivo tumor formation, and caused cell cycle arrest. miR-186 mimics also 
inhibited the migration and invasion of CCLP1 and SG-231 cells. Mechanistically, the 3′-untranslated region 
(3′-UTR) of Twist1 mRNA is a direct target of miR-186. Further, miR-186 inhibited the expressions of Twist1, 
N-cadherin, vimentin, and matrix metallopeptidase 9 (MMP9) proteins, whereas it increased the expression of 
E-cadherin in CCLP1 and SG-231 cells. Silencing of Twist1 expression enhanced the inhibitory effects of miR-
186 on the proliferation, migration, and invasion of CCLP1 and SG-231 cells. In conclusion, miR-186 inhibited 
cell proliferation, migration, invasion, and epithelial–mesenchymal transition (EMT) through targeting Twist1 
in human CCA. Thus, miR-186/Twist1 axis may benefit the development of therapies for CCA.},
DOI = {10.3727/096504019X15565325878380}
}