Skip Navigation


ToxSci Advance Access originally published online on July 21, 2008
Toxicological Sciences 2008 105(2):303-311; doi:10.1093/toxsci/kfn141
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrowOA All Versions of this Article:
105/2/303    most recent
kfn141v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Sotoca Covaleda, A. M.
Right arrow Articles by Murk, A. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Sotoca Covaleda, A. M.
Right arrow Articles by Murk, A. J.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The Author 2008. Published by Oxford University Press on behalf of the Society of Toxicology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org
The online version of this article has been published under an open access model. Users are entitled to use, reproduce, disseminate, or display the open access version of this article for non-commercial purposes provided that: the original authorship is properly and fully attributed; the Journal and Oxford University Press are attributed as the original place of publication with the correct citation details given; if an article is subsequently reproduced or disseminated not in its entirety but only in part or as a derivative work this must be clearly indicated. For commercial re-use, please contact journals.permissions@oxfordjournals.org

Influence of Cellular ER{alpha}/ERβ Ratio on the ER{alpha}-Agonist Induced Proliferation of Human T47D Breast Cancer Cells

Ana Maria Sotoca Covaleda*,1, Hans van den Berg*, Jacques Vervoort{dagger}, Paul van der Saag{ddagger}, Anders Ström§, Jan-Åke Gustafsson§, Ivonne Rietjens* and Albertinka J. Murk*

* Toxicology section, Wageningen University, Tuinlaan 5, 6703 HE, Wageningen, The Netherlands {dagger} Department of Biochemistry, Wageningen University, Dreijenlaan 3, 6703 HA, Wageningen, The Netherlands {ddagger} Hubrecht Institute, Uppsalalaan 8, 3584 CT, Utrecht, The Netherlands § Department of Biosciences and Nutrition, Karolinska Institute, Novum, 14186 Huddinge, Sweden

1 To whom correspondence should be addressed. Fax: +31-317484931. E-mail: ana.sotoca{at}wur.nl.

Received March 26, 2008; accepted July 7, 2008


  Abstract

Breast cancer cells show overexpression of estrogen receptor (ER) {alpha} relative to ERβ compared to normal breast tissues. This observation has lead to the hypothesis that ERβ may modulate the proliferative effect of ER{alpha}. This study investigated how variable cellular expression ratios of the ER{alpha} and ERβ modulate the effects on cell proliferation induced by ER{alpha} or ERβ agonists, respectively. Using human osteosarcoma (U2OS) ER{alpha} or ERβ reporter cells, propyl-pyrazole-triol (PPT) was shown to be a selective ER{alpha} and diarylpropionitrile (DPN) a preferential ERβ modulator. The effects of these selective estrogen receptor modulators (SERMs) and of the model compound E2 on the proliferation of T47D human breast cancer cells with tetracycline-dependent expression of ERβ (T47D-ERβ) were characterized. E2-induced cell proliferation of cells in which ERβ expression was inhibited was similar to that of the T47D wild-type cells, whereas this E2-induced cell proliferation was no longer observed when ERβ expression in the T47D-ERβ cells was increased. In the T47D-ERβ cell line, DPN also appeared to be able to suppress cell proliferation when levels of ERβ expression were high. In the T47D-ERβ cell line, PPT was unable to suppress cell proliferation at all ratios of ER{alpha}/ERβ expression, reflecting its ability to activate only ER{alpha} and not ERβ. It is concluded that effects of estrogen-like compounds on cell proliferation are dependent on the actual ER{alpha}/ERβ expression levels in these cells or tissues and the potential of the estrogen agonists to activate ER{alpha} and/or ERβ.

Key Words: estrogen receptors; SERM; breast cancer cells; T47D-ERβ; inducible; ER-U2OS-Luc.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Nucleic Acids ResHome page
N. S. Wickramasinghe, T. T. Manavalan, S. M. Dougherty, K. A. Riggs, Y. Li, and C. M. Klinge
Estradiol downregulates miR-21 expression and increases miR-21 target gene expression in MCF-7 breast cancer cells
Nucleic Acids Res., May 1, 2009; 37(8): 2584 - 2595.
[Abstract] [Full Text] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.