The Hairy and Enhancer of Split homologue-1 (HES-1) mediates the proliferative effect of 17β-estradiol on breast cancer cell lines

Anders Ström, Naoya Arai, Jörg Leers, Jan Åke Gustafsson

Research output: Contribution to journalArticlepeer-review

38 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)5951-5953
Number of pages3
JournalOncogene
Volume19
Issue number51
DOIs
StatePublished - Nov 30 2000

Keywords

  • 17β-estradiol
  • Antiestrogen
  • HES-1
  • PCNA
  • Proliferation

ASJC Scopus subject areas

  • Molecular Biology
  • Cancer Research
  • Genetics

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