S100A6 promotes proliferation of intrahepatic cholangiocarcinoma cells via the activation of the p38/MAPK pathway-Reference-Cited by-同舟云学术

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

Published:2017-10 Issue:23 Volume:13 Page:2053-2063
ISSN:1479-6694
Container-title:Future Oncology
language:en
Short-container-title:Future Oncology

Author:

Zheng Susu¹,Shen Hujia¹,Jia Qingan¹,Jing Chuyu¹,Lin Jiajia¹,Zhang Meixia¹,Zhang Xiaolei²,Zhang Boheng¹,Liu Yinkun¹

Affiliation:

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.

Publisher

Future Medicine Ltd

Subject

Cancer Research,Oncology,General Medicine

Link

https://www.futuremedicine.com/doi/pdf/10.2217/fon-2017-0199

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