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

doi:10.1038/sj.onc.1203990

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 journal › Article › peer-review

39 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 language	English (US)
Pages (from-to)	5951-5953
Number of pages	3
Journal	Oncogene
Volume	19
Issue number	51
DOIs	https://doi.org/10.1038/sj.onc.1203990
State	Published - Nov 30 2000

Keywords

17β-estradiol
Antiestrogen
HES-1
PCNA
Proliferation

ASJC Scopus subject areas

Molecular Biology
Cancer Research
Genetics

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

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.",

keywords = "17β-estradiol, Antiestrogen, HES-1, PCNA, Proliferation",

author = "Anders Str{\"o}m and Naoya Arai and J{\"o}rg Leers and Gustafsson, {Jan {\AA}ke}",

note = "Funding Information: 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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AU - Ström, Anders

AU - Arai, Naoya

AU - Leers, Jörg

AU - Gustafsson, Jan Åke

N1 - Funding Information: 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.

PY - 2000/11/30

Y1 - 2000/11/30

N2 - 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.

AB - 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.

KW - 17β-estradiol

KW - Antiestrogen

KW - HES-1

KW - PCNA

KW - Proliferation

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

Abstract

Keywords

ASJC Scopus subject areas

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