miR-186 Suppresses the Progression of Cholangiocarcinoma Cells Through Inhibition of Twist1 |
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Authors: | Ming Zhang Baochang Shi Kai Zhang |
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Institution: | Department of Hepatobiliary Surgery, Shandong Provincial Third Hospital, Jinan, Shandong, P.R. China |
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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. |
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Keywords: | miR-186 Cholangiocarcinoma (CCA) Twist1 E-cadherin |
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