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Future Oncol. 2017 Oct;13(23):2053-2063. doi: 10.2217/fon-2017-0199. Epub 2017 Oct 6.

S100A6 promotes proliferation of intrahepatic cholangiocarcinoma cells via the activation of the p38/MAPK pathway.

Author information

1
Department of Hepatic Oncology, Liver Cancer Institute & Zhongshan Hospital, Fudan University, Shanghai 20032, PR China.
2
Department of Pathology, Zhongshan hospital, Fudan University, Shanghai 20032, PR China.

Abstract

AIM:

We explored the expression of S100A6 and its role in intrahepatic cholangiocarcinoma (ICC).

METHODS:

The expression of S100A6 in ICC samples was detected by immunohistochemistry. In vitro experiments, we silenced and overexpressed S100A6 to investigate its role in cell functions.

RESULTS:

The expression of S100A6 was markedly increased in ICC tissues and cell lines. S100A6 overexpression was an independent risk factor for patients' survival. Silencing S100A6 resulted in a suppression of proliferation and p38/MAPK activity, while overexpressing S100A6 caused a promotion of proliferation and p38/MAPK.

DISCUSSION:

 S100A6 participated in the proliferation of ICC cells and correlated with a more aggressive behavior of ICC. Conclusion: S100A6 may serve as a novel prognostic marker and a potential therapeutic target for ICC patients.

KEYWORDS:

S100A6; intrahepatic cholangiocarcinoma; prognosis; proliferation

PMID:
28984474
DOI:
10.2217/fon-2017-0199
[Indexed for MEDLINE]

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