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Future Oncol. 2018 Apr;14(9):837-847. doi: 10.2217/fon-2017-0534. Epub 2018 Mar 23.

S100A11 promotes TGF-β1-induced epithelial-mesenchymal transition through SMAD2/3 signaling pathway in intrahepatic cholangiocarcinoma.

Author information

1
Liver Cancer Institute & Zhongshan Hospital of Fudan University, Shanghai 200032, PR China.
2
Center for Evidence-Based Medicine, Fudan University, Shanghai 200032, PR China.

Abstract

AIM:

Our previous study found S100A11 was significantly raised in intrahepatic cholangiocarcinoma cells, but the relationship between S100A11 and intrahepatic cholangiocarcinoma remains unclear.

METHODS:

We investigated the effect of silencing S100A11 on TGF-β1-induced epithelial-mesenchymal transition (EMT), cell migration and invasion.

RESULTS:

Our results demonstrated silencing S100A11 inhibited TGF-β1-induced cell migration, invasion and EMT, expression of EMT markers E-cadherin, N-cadherin, β-catenin, vimentin, Slug and Snail was reversed. Furthermore, TGF-β1-induced p-SMAD2 and 3 were also inhibited due to low S100A11 expression.

CONCLUSION:

Our present study indicated that S100A11 promotes EMT through accumulation of TGF-β1 expression, and TGF-β1-induced upregulation of p-SMAD2 and 3.

KEYWORDS:

EMT; intrahepatic cholangiocarcinoma; invasion

PMID:
29569474
DOI:
10.2217/fon-2017-0534
[Indexed for MEDLINE]
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