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