Abstract
The mechanism behind hormone dependent growth of breast cancer is presently not well understood. We show that the 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. In T47D cells with inducible exogenous HES-1 expression, induced expression of HES-1 protein prevented the proliferative effect of 17β-estradiol and subsequent up regulation of proliferating cell nuclear antigen (PCNA). An inverse correlation between the HES-1 and PCNA protein levels respectively was found in colon cancer cell lines. These findings point to a potential role of HES-1 as a tumor suppressor in epithelial cells, and as a mediator of 17β-estradiols proliferative effect on breast cancer cells.
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Acknowledgements
This study was supported by grant from the Swedish Cancer Fund and from Karo Bio AB. We thank Dr Michael Caudy (Weill Medical College of Cornell University) for providing HES-1 expression constructs.
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Ström, A., Arai, N., Leers, J. et al. The Hairy and Enhancer of Split homologue-1 (HES-1) mediates the proliferative effect of 17β-estradiol on breast cancer cell lines. Oncogene 19, 5951–5953 (2000). https://doi.org/10.1038/sj.onc.1203990
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DOI: https://doi.org/10.1038/sj.onc.1203990
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