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Cancers 2011, 3(3), 2990-3001; doi:10.3390/cancers3032990
Article

β-Catenin Is a Positive Regulator of Estrogen Receptor-α Function in Breast Cancer Cells

,
,
 and
*
Hormones and Signal Transduction Group, German Cancer Research Center (DKFZ), DKFZ-ZMBH Alliance, Im Neuenheimer Feld 581, 69120 Heidelberg, Germany
* Author to whom correspondence should be addressed.
Received: 9 June 2011 / Revised: 18 July 2011 / Accepted: 19 July 2011 / Published: 22 July 2011
(This article belongs to the Special Issue Cancer Signaling Pathways and Crosstalk)
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Abstract

Estrogen receptor-alpha (ERα) is a key factor in the development of breast cancer in humans. The expression and activity of ERα is regulated by a multitude of intracellular and extracellular signals. Here we show a cross-talk between β-catenin and ERα in human breast cancer cells. Knockdown of β-catenin by RNAi resulted in significant reduction of ERα mRNA and/or protein levels in MCF-7, T-47D, and BT-474 breast cancer cells and in significant reduction of estradiol-induced expression of the ERα target genes pS2 and GREB1. In addition β-catenin silencing resulted in significant decrease of growth of MCF-7 cells both in the absence and presence of estradiol. β-catenin and ERα could not be co-immunoprecipitated by ERα antibodies from lysates of E2-treated or untreated cells suggesting lack of direct physical interaction. It is concluded that β-catenin is a positive regulator of ERα mRNA and protein expression.
Keywords: β-catenin; estrogen receptor; cross-talk; gene expression; transcriptional activity; breast cancer cell β-catenin; estrogen receptor; cross-talk; gene expression; transcriptional activity; breast cancer cell
This is an open access article distributed under the Creative Commons Attribution License (CC BY 3.0).

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Gupta, N.; Schmitt, F.; Grebhardt, S.; Mayer, D. β-Catenin Is a Positive Regulator of Estrogen Receptor-α Function in Breast Cancer Cells. Cancers 2011, 3, 2990-3001.

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