Hairy and enhancer of split homolog-1 (HES-1) mediates the proliferative effect of Beta-estradiol on breast cancer cell lines
KeywordsBreast Cancer Colon Cancer Breast Cancer Cell Tamoxifen Breast Cancer Cell Line
The mechanism behind estradiol-dependent growth of breast cancer is presently not well understood. We show that the hairy and enhancer of split homolog-1 (HES-1) protein level in the breast cancer cell lines T47D and MCF-7 is down-regulated by 17β-estradiol treatment. This regulation could be reversed by addition of the anti-estrogens 4OH tamoxifen, raloxifen and Imperial Chemical Industries (ICI) 182,780. Furthermore, T47D cells with inducible exogenous HES-1 expression showed that HES-1 protein needs to be removed in order for 17β-estradiol to have a proliferative effect and subsequently up-regulating proliferating cell nuclear antigen (PCNA).
An inverse correlation between the protein levels of HES-1 and PCNA was found in colon cancer cell lines. These findings point to a role of HES-1 as a tumor suppressor in epithelial cells, and as a target for 17β-estradiol in breast cancer cells. Present findings makes HES-1 useful for diagnosis and an interesting target for cancer treatment.