S100A6 通过激活 p38/MAPK 通路促进肝内胆管癌细胞的增殖。
S100A6 promotes proliferation of intrahepatic cholangiocarcinoma cells via the activation of the p38/MAPK pathway.
机构信息
Department of Hepatic Oncology, Liver Cancer Institute & Zhongshan Hospital, Fudan University, Shanghai 20032, PR China.
Department of Pathology, Zhongshan hospital, Fudan University, Shanghai 20032, PR China.
出版信息
Future Oncol. 2017 Oct;13(23):2053-2063. doi: 10.2217/fon-2017-0199. Epub 2017 Oct 6.
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.
目的
探讨 S100A6 在肝内胆管癌（ICC）中的表达及其作用。
方法
采用免疫组织化学法检测 ICC 组织中 S100A6 的表达。体外实验沉默和过表达 S100A6，研究其在细胞功能中的作用。
结果
S100A6 在 ICC 组织和细胞系中表达明显增加。S100A6 过表达是患者生存的独立危险因素。沉默 S100A6 导致增殖和 p38/MAPK 活性受到抑制，而过表达 S100A6 则促进增殖和 p38/MAPK。
讨论
S100A6 参与 ICC 细胞的增殖，并与 ICC 更具侵袭性行为相关。
结论
S100A6 可能成为 ICC 患者新的预后标志物和潜在治疗靶点。
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