S100A11 promotes

Our previous study found S100A11 was significantly raised in intrahepatic cholangiocarcinoma cells, but the relationship between S100A11 and intrahepatic cholangiocarcinoma remains unclear. We investigated the effect of silencing S100A11 on -induced epithelial-mesenchymal transition (EMT), cell migr...

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Bibliographic Details
Published inFuture oncology (London, England)
Main Authors Zhang, Meixia, Zheng, Susu, Jing, Chuyu, Zhang, Juan, Shen, Hujia, Xu, Xin, Lin, Jiajia, Zhang, Boheng
Format Journal Article
LanguageEnglish
Published Future Medicine Ltd 01.03.2018
Subjects
EMT
intrahepatic cholangiocarcinoma
invasion
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Summary:Our previous study found S100A11 was significantly raised in intrahepatic cholangiocarcinoma cells, but the relationship between S100A11 and intrahepatic cholangiocarcinoma remains unclear. We investigated the effect of silencing S100A11 on -induced epithelial-mesenchymal transition (EMT), cell migration and invasion. Our results demonstrated silencing S100A11 inhibited -induced cell migration, invasion and EMT, expression of EMT markers E-cadherin, N-cadherin, β-catenin, vimentin, Slug and Snail was reversed. Furthermore, -induced and were also inhibited due to low S100A11 expression. Our present study indicated that S100A11 promotes EMT through accumulation of expression, and -induced upregulation of and .
ISSN:1479-6694
1744-8301
DOI:10.2217/fon-2017-0534