help button home button Endocrine Society Molecular Endocrinology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
This version published online on April 27, 2006
Molecular Endocrinology, doi:10.1210/me.2005-0063
A more recent version of this article appeared on September 1, 2006
This Article
Right arrow Author Manuscript (PDF)
Right arrow All Versions of this Article:
20/9/2020    most recent
Author Manuscript (PDF)
Right arrow Purchase Article
Right arrow View Shopping Cart
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 Download to citation manager
Right arrow NURSA Molecule Pages Link
Right arrow Request Copyright Permission
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Cui, Y.
Right arrow Articles by Fuqua, S. A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Cui, Y.
Right arrow Articles by Fuqua, S. A.

Submitted on January 25, 2005
Accepted on April 17, 2006

Metastasis-Associated Protein 2 is a Repressor of Estrogen Receptor {alpha} Whose Overexpression Leads to Estrogen-Independent Growth of Human Breast Cancer Cells

Yukun Cui, Airu Niu, Richard Pestell, Rakesh Kumar, Edward M. Curran, Yunde Liu, and Suzanne AW Fuqua*

Departments of Medicine, Breast Center, Molecular and Cellular Biology, Baylor College of Medicine, and the Methodist Hospital, One Baylor Plaza, Houston, TX 77030; Department of Cancer Biology, Kimmel Cancer Center, Thomas Jefferson University, Phildadelphia, PA 19107; Department of Molecular and Cellular Oncology, University of Texas M. D. Anderson Cancer Center, Houston, TX 77030; Department of Pediatrics and the Sealy Vaccine Center, University of Texas Medical Branch, Children's Hospital, Galveston, TX; Department of Medical Laboratory Techniques, Tianjin Medical University, One Guangdong Road, Tianjin, China

* To whom correspondence should be addressed. E-mail: sfuqua{at}breastcenter.tmc.edu.

Estrogen Receptor (ER) {alpha} activity is controlled by the balance of coactivators and corepressors contained within cells which are recruited into transcriptional complexes. The metastasis associated (MTA) family of proteins have been demonstrated to be associated with breast tumor cell progression and ER{alpha} activity. We demonstrate that MTA2 expression is correlated with ER{alpha} protein expression in invasive breast tumors. We show that the MTA2 family member can bind to ER{alpha} and repress its activity in human breast cancer cells. Furthermore, it can inhibit ER{alpha} mediated colony formation and render breast cancer cells resistant to estradiol and the growth-inhibitory effects of the antiestrogen tamoxifen. MTA2 participates in the deacetylation of ER{alpha} protein, potentially through its associated HDAC1 activity. We hypothesize that MTA2 is a repressor of ER{alpha} activity and that it could represent a new therapeutic target of ER{alpha} action in human breast tumors.
Key words: Estrogen receptor alpha • Breast Cancer • Endocrine Therapy • Protein Acetylation • Repressor • HDAC

NURSA Molecule Pages Link:

Nuclear Receptors:   ERα
Coregulators:   PGC-1  |  L7/SPA  |  SAF-B  |  MTA2  |  ERBP  |  MICoA
Ligands:   17β-Estradiol  |  9-cis-Retinoic acid  |  R1881  |  R5020  |  Fulvestrant



This article has been cited by other articles:


Home page
 J. Biol. Chem.Home page
B. Manavathi and R. Kumar
Metastasis Tumor Antigens, an Emerging Family of Multifaceted Master Coregulators
J. Biol. Chem., January 19, 2007; 282(3): 1529 - 1533.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
Endocrinology Endocrine Reviews J. Clin. End. & Metab.
Molecular Endocrinology Recent Prog. Horm. Res. All Endocrine Journals
Copyright © 2006 by The Endocrine Society