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A more recent version of this article appeared on April 19, 2002
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M110051200v1
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Papers In Press, published online ahead of print February 13, 2002
J. Biol. Chem, 10.1074/jbc.M110051200
Submitted on October 18, 2001
Revised on January 29, 2002
Accepted on February 12, 2002

Modulation of estrogen receptor-mediated transactivation by orphan receptor TR4 in MCF-7 cells

Chih-Rong Shyr, Yueh-Chiang Hu, Eungseok Kim, and Chawnshang Chang

Department of Pathology, University of Rochester Medical Center, Rochester, NY 14642

Corresponding Author: chang{at}urmc.rochester.edu

The human testicular orphan receptor 4 (TR4) is a member of the nuclear receptor superfamily that shows a broad tissue distribution with higher expression in the nervous system and male reproductive tract. TR4 functions as a transcriptional modulator that controls various target genes via binding to the DNA hormone response elements. Here we report that instead of direct binding to hormone response elements for gene regulation, TR4 can also go through direct protein-protein interaction to repress estrogen receptor (ER)-mediated transactivation. Electrophoretic mobility shift and GST pull-down clearly demonstrate that the direct interaction between TR4 and ER will inhibit the homodimerization of ER and interrupt/prevent ER binding to the estrogen response element. The consequence of these events may then result in the suppression of ER target genes, such as cyclin D1 and pS2 and inhibition of ER-mediated cell proliferation in the MCF-7 cells stably transfected with TR4. Together, our results showing that TR4 can suppress ER function via protein-protein interaction not only represent an unique cross-talk signaling pathway in the nuclear receptor superfamily, it may also provide us a new strategy to modulate ER function in the breast cancer cells.


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