Estrogen receptor alpha inhibits p53-mediated transcriptional repression: implications for the regulation of apoptosis.

Estrogen receptor alpha inhibits p53-mediated transcriptional repression: implications for the regulation of apoptosis. Research Abstract Details 

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Estrogen receptor alpha inhibits p53-mediated transcriptional repression: implications for the regulation of apoptosis. Abstract Text:

Aejaz Sayeed,Santhi D Konduri,Wensheng Liu,Sanjay Bansal,Fengzhi Li,Gokul M Das,

Estrogen receptor alpha (ERalpha) and tumor suppressor protein p53 exert opposing effects on cellular proliferation. As a transcriptional regulator, p53 is capable of activating or repressing various target genes. We have previously reported that ERalpha binds directly to p53, leading to down-regulation of transcriptional activation by p53. In addition to transcriptional activation, transcriptional repression of a subset of target genes by p53 plays important roles in diverse biological processes, such as apoptosis. Here, we report that ERalpha inhibits p53-mediated transcriptional repression. Chromatin immunoprecipitation assays reveal that ERalpha interacts in vivo with p53 bound to promoters of Survivin and multidrug resistance gene 1, both targets for transcriptional repression by p53. ERalpha binding to p53 leads to inhibition of p53-mediated transcriptional regulation of these genes in human cancer cells. Transcriptional derepression of Survivin by ERalpha is dependent on the p53-binding site on the Survivin promoter, consistent with our observation that p53 is necessary for ERalpha to access the promoters. Importantly, mutagenic conversion of this site to an activation element enabled ERalpha to repress p53-mediated transcriptional activation. Further, RNA interference-mediated knockdown of ERalpha resulted in reduced Survivin expression and enhanced the propensity of MCF-7 cells to undergo apoptosis in response to staurosporine treatment, an effect that was blocked by exogenous expression of Survivin. These results unravel a novel mechanism by which ERalpha opposes p53-mediated apoptosis in breast cancer cells. The findings could have translational implications in developing new therapeutic and prevention strategies against breast cancer.

Estrogen receptor alpha inhibits p53-mediated transcriptional repression: implications for the regulation of apoptosis. Publishing Authors By Initials

A Sayeed,SD Konduri,W Liu,S Bansal,F Li,GM Das,

For similar proteins: dna-binding proteins: tumor suppressor protein p53 research abstracts see: proteins: dna-binding proteins: tumor suppressor protein p53 research

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Estrogen receptor alpha inhibits p53-mediated transcriptional repression: implications for the regulation of apoptosis. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: Cancer research

VOLUME: 67

Page Numbers: 7746-55

Journal Abbreviation: Cancer Res.

ISSN: 0008-5472

DAY: 15

MONTH: Aug

YEAR: 2007

Estrogen receptor alpha inhibits p53-mediated transcriptional repression: implications for the regulation of apoptosis. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 2984705

Estrogen receptor alpha inhibits p53-mediated transcriptional repression: implications for the regulation of apoptosis. Keywords Mesh Terms:

KEYWORDS: Tumor Suppressor Protein p53

MESH TERMS: metabolism

Chemical & Substance for Abstract: Estrogen receptor alpha inhibits p53-mediated transcriptional repression: implications for the regulation of apoptosis. Information

Substance Name: Histone Deacetylases

Registry Number: EC 3.5.1.-

Grant and Affiliation Information for Estrogen receptor alpha inhibits p53-mediated transcriptional repression: implications for the regulation of apoptosis.

AFFILIATION: Department of Pharmacology and Therapeutics, Roswell Park Cancer Institute, Buffalo, New York 14263, USA.

Country: United States

AGENCY: United States NCI

GRANT: CA079911

ACRONYM: CA

MEDLINETA: Cancer Res

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