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

来源：

FUTURE ONCOLOGY | 2017年 / 13卷 / 23期

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

页码：2053 / 2063

页数：11

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