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Abstract
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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.