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Breast Cancer Research

, 2:P2.03 | Cite as

Hairy and enhancer of split homolog-1 (HES-1) mediates the proliferative effect of Beta-estradiol on breast cancer cell lines

  • A Ström
  • N Arai
  • J Leers
  • J-Å Gustafsson
Meeting abstract

Keywords

Breast Cancer Colon Cancer Breast Cancer Cell Tamoxifen Breast Cancer Cell Line 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Full text

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.

Copyright information

© Current Science Ltd 2000

Authors and Affiliations

  • A Ström
    • 1
  • N Arai
    • 1
  • J Leers
    • 1
  • J-Å Gustafsson
    • 1
  1. 1.Karolinska Institutet, Department of Biosciences at NovumHuddingeSweden

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