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This version published online on September 9, 2004
Molecular Endocrinology, doi:10.1210/me.2004-0258
Molecular Endocrinology Vol. 0, No. 2004 200402581-
doi:10.1210/me.2004-0258
Copyright © 2004 by the Endocrine Society.
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*Breast Cancer

Submitted on June 28, 2004
Accepted on August 30, 2004

Hormonal regulation of MTA3 transcription in breast cancer cells

Naoyuki Fujita, Masahiro Kajita, Panya Taysavang, and Paul A. Wade*

Department of Pathology and Laboratory Medicine, Winship Cancer Institute, Emory University, Atlanta, GA, USA

* To whom correspondence should be addressed. E-mail: pwade{at}emory.edu.

Metastasis associated protein 3 (MTA3) is a cell type specific subunit of the Mi-2/NuRD transcriptional corepressor complex. In breast cancer cells, MTA3 and the Mi-2/NuRD complex mediate repression of Snail, a transcription factor that promotes epithelial to mesenchymal transitions. Thus, MTA3 functions to maintain a differentiated, epithelial status in breast cancer. Interestingly, in mammary epithelial cells, MTA3 biosynthesis requires both functional estrogen receptor and estradiol. Here we have investigated the molecular basis for estrogen and estrogen receptor-dependent expression of MTA3 in breast cancer cells. Molecular dissection of the MTA3 promoter using transient transfection assays identified a composite element required for high-level transcription consisting of an SP1 site in close proximity to a consensus ERE half-site. Depletion of either SP1 or ER-{alpha} by RNAi led to loss of MTA3 transcript in multiple breast cancer cell lines, indicating a requirement for both transcription factors in expression of endogenous MTA3. The MTA3 gene thus joins a growing list of loci regulated by both SP1 and estrogen receptor.
Key words: estrogen receptor • SP1 • transcription factor • MTA3

NURSA Molecule Pages Link:

Nuclear Receptors:   ERα
Coregulators:   MTA2  |  MTA1
Ligands:   17β-Estradiol



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