HES1 overexpression promotes cell proliferation and invasion in breast cancer and predicts poor survival.

HES1 is a transcriptional repressor involved in cell differentiation and proliferation, but the expression pattern and biological roles of HES1 in breast cancer have not been examined. In this study, we examined HES1 expression in breast cancer tissues using immunohistochemistry and western blot analyses and investigated HES1 function using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and Matrigel invasion assays. Significant relationships were observed between HES1 upregulation and advanced tumour-node-metastasis stage (p = 0.011), node metastasis (p = 0.043), negative oestrogen receptor expression (p = 0.001) and triple-negative status (p = 0.001). HES1 overexpression was correlated with poor prognosis in breast cancer patients (p < 0.05), and the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and Matrigel invasion assays showed that silencing HES1 in MDA-MB-231 cells decreased cell proliferation and invasion, whereas overexpression of HES1 in MCF-7 cells enhanced cell proliferation and invasion. Further analyses showed that silencing HES1 downregulated p-AKT and impeded the epithelial-mesenchymal transition, whereas overexpression of HES1 upregulated AKT phosphorylation and induced epithelial-mesenchymal transition. Our study demonstrated that HES1 upregulation is a predictor of poor prognosis in human breast cancers and might be a critical contributor to the proliferation and invasion of breast cancer cells. Moreover, the proportion of HES1 overexpression in triple-negative breast cancer samples was significantly higher. Thus, HES1 might be a potential therapeutic target in the treatment of triple-negative breast cancer.