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

被引:13
|
作者
Zheng, Susu [1 ,2 ]
Shen, Hujia [1 ,2 ]
Jia, Qingan [1 ,2 ]
Jing, Chuyu [1 ,2 ]
Lin, Jiajia [1 ,2 ]
Zhang, Meixia [1 ,2 ]
Zhang, Xiaolei [3 ]
Zhang, Boheng [1 ,2 ]
Liu, Yinkun [1 ,2 ]
机构
[1] Fudan Univ, Liver Canc Inst, Dept Hepat Oncol, Shanghai 20032, Peoples R China
[2] Fudan Univ, Zhongshan Hosp, Shanghai 20032, Peoples R China
[3] Fudan Univ, Zhongshan Hosp, Dept Pathol, Shanghai 20032, Peoples R China
基金
中国国家自然科学基金;
关键词
intrahepatic cholangiocarcinoma; prognosis; proliferation; S100A6; HUMAN HEPATOCELLULAR-CARCINOMA; GASTRIC-CANCER; THERAPEUTIC TARGET; MAPK PATHWAYS; EXPRESSION; PROTEIN; KINASE; CALCYCLIN; MIGRATION; GROWTH;
D O I
10.2217/fon-2017-0199
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
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.
引用
收藏
页码:2053 / 2063
页数:11
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