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S100A11 通过 SMAD2/3 信号通路促进 TGF-β1 诱导的肝内胆管癌上皮-间充质转化。

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

机构信息

Liver Cancer Institute & Zhongshan Hospital of Fudan University, Shanghai 200032, PR China.

Center for Evidence-Based Medicine, Fudan University, Shanghai 200032, PR China.

出版信息

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

DOI:10.2217/fon-2017-0534
PMID:29569474
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.

摘要

目的

我们之前的研究发现 S100A11 在肝内胆管癌细胞中显著升高，但 S100A11 与肝内胆管癌之间的关系尚不清楚。

方法

我们研究了沉默 S100A11 对 TGF-β1 诱导的上皮-间充质转化（EMT）、细胞迁移和侵袭的影响。

结果

我们的结果表明，沉默 S100A11 抑制了 TGF-β1 诱导的细胞迁移、侵袭和 EMT，EMT 标志物 E-钙黏蛋白、N-钙黏蛋白、β-连环蛋白、波形蛋白、Slug 和 Snail 的表达也被逆转。此外，由于 S100A11 表达水平较低，TGF-β1 诱导的 p-SMAD2 和 3 也被抑制。

结论

本研究表明，S100A11 通过积累 TGF-β1 的表达以及 TGF-β1 诱导的 p-SMAD2 和 3 的上调，促进 EMT。

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