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Molecular Endocrinology
Article . 2006 . Peer-reviewed
Data sources: Crossref
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Metastasis-Associated Protein 2 Is a Repressor of Estrogen Receptor α Whose Overexpression Leads to Estrogen-Independent Growth of Human Breast Cancer Cells

Authors: Yunde Liu; Richard G. Pestell; Yukun Cui; Rakesh Kumar; Suzanne A. W. Fuqua; Edward M. Curran; Airu Niu;

Metastasis-Associated Protein 2 Is a Repressor of Estrogen Receptor α Whose Overexpression Leads to Estrogen-Independent Growth of Human Breast Cancer Cells

Abstract

Estrogen receptor (ER)alpha activity is controlled by the balance of coactivators and corepressors contained within cells that are recruited into transcriptional complexes. The metastasis-associated protein (MTA) family has been demonstrated to be associated with breast tumor cell progression and ERalpha activity. We demonstrate that MTA2 expression is correlated with ERalpha protein expression in invasive breast tumors. We show that the MTA2 family member can bind to ERalpha and repress its activity in human breast cancer cells. Furthermore, it can inhibit ERalpha-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 ERalpha protein, potentially through its associated histone deacetylase complex 1 activity. We hypothesize that MTA2 is a repressor of ERalpha activity and that it could represent a new therapeutic target of ERalpha action in human breast tumors.

Keywords

Binding Sites, Transcription, Genetic, Lysine, Estrogen Receptor alpha, Acetylation, Breast Neoplasms, Estrogens, Histone Deacetylases, Repressor Proteins, Cell Line, Tumor, Mutation, Humans, Cell Proliferation, Protein Binding

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citations
This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Citations provided by BIP!
popularity
This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
BIP!Popularity provided by BIP!
influence
This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Influence provided by BIP!
impulse
This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.
BIP!Impulse provided by BIP!
68
Top 10%
Top 10%
Top 10%
bronze