Genetic ablation of the amplified-in-breast cancer 1 inhibits spontaneous prostate cancer progression in mice.

Genetic ablation of the amplified-in-breast cancer 1 inhibits spontaneous prostate cancer progression in mice. Research Abstract Details 

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Genetic ablation of the amplified-in-breast cancer 1 inhibits spontaneous prostate cancer progression in mice. Abstract Text:

Arthur C-K Chung,Suoling Zhou,Lan Liao,Jean Ching-Yi Tien,Norman M Greenberg,Jianming Xu,

Although the amplified-in-breast cancer 1 (AIB1; SRC-3, ACTR, or NCoA3) was defined as a coactivator for androgen receptor (AR) by in vitro studies, its role in AR-mediated prostate development and prostate cancer remained unexplored. We report here that AIB1 is expressed in the basal and stromal cells but not in the epithelial cells of the normal mouse prostates. AIB1 deficiency only slightly delayed prostate growth and had no effect on androgen-dependent prostate regeneration, suggesting an unessential role of AIB1 in AR function in the prostate. Surprisingly, when prostate tumorigenesis was induced by the SV40 transgene in transgenic adenocarcinoma of the mouse prostate (TRAMP) mice, AIB1 expression was observed in certain epithelial cells of the prostate intraepithelial neoplasia (PIN) and well-differentiated carcinoma and in almost all cells of the poorly differentiated carcinoma. After AIB1 was genetically inactivated in AIB1-/-/TRAMP mice, the progression of prostate tumorigenesis in most AIB1-/-/TRAMP mice was arrested at the well-differentiated carcinoma stage. Wild-type (WT)/TRAMP mice developed progressive, multifocal, and metastatic prostate tumors and died between 25 and 34 weeks. In contrast, AIB1-/-/TRAMP mice only exhibited PIN and early-stage well-differentiated carcinoma by 39 weeks. AIB1-/-/TRAMP prostates showed much lower cell proliferation than WT/TRAMP prostates. Most AIB1-/-/TRAMP mice could survive more than 35 weeks and died with other types of tumors or unknown reasons. Our results indicate that induction of AIB1 expression in partially transformed epithelial cells is essential for progression of prostate tumorigenesis into poorly differentiated carcinoma. Inhibition of AIB1 expression or function in the prostate epithelium may be a potential strategy to suppress prostate cancer initiation and progression.

Genetic ablation of the amplified-in-breast cancer 1 inhibits spontaneous prostate cancer progression in mice. Publishing Authors By Initials

AC Chung,S Zhou,L Liao,JC Tien,NM Greenberg,J Xu,

For similar proteins: dna-binding proteins: trans-activators research abstracts see: proteins: dna-binding proteins: trans-activators research

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Genetic ablation of the amplified-in-breast cancer 1 inhibits spontaneous prostate cancer progression in mice. Journal Published:

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

Journal: Cancer research

VOLUME: 67

Page Numbers: 5965-75

Journal Abbreviation: Cancer Res.

ISSN: 0008-5472

DAY: 15

MONTH: Jun

YEAR: 2007

Genetic ablation of the amplified-in-breast cancer 1 inhibits spontaneous prostate cancer progression in mice. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 2984705

Genetic ablation of the amplified-in-breast cancer 1 inhibits spontaneous prostate cancer progression in mice. Keywords Mesh Terms:

KEYWORDS: Trans-Activators

MESH TERMS: metabolism

Chemical & Substance for Abstract: Genetic ablation of the amplified-in-breast cancer 1 inhibits spontaneous prostate cancer progression in mice. Information

Substance Name: nuclear receptor coactivator 3

Registry Number: EC 2.3.1.48

Grant and Affiliation Information for Genetic ablation of the amplified-in-breast cancer 1 inhibits spontaneous prostate cancer progression in mice.

AFFILIATION: Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, Texas 77030, USA.

Country: United States

AGENCY: United States NIDDK

GRANT: DK58242

ACRONYM: DK

MEDLINETA: Cancer Res

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