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

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

Future Oncol. 2018 Mar 23;:

Authors: Zhang M, Zheng S, Jing C, Zhang J, Shen H, Xu X, Lin J, Zhang B

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.

PMID: 29569474 [PubMed - as supplied by publisher]

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