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Papers In Press, published online ahead of print January 15, 2002
J. Biol. Chem, 10.1074/jbc.M111962200
Submitted on December 14, 2001
Revised on January 8, 2002
Accepted on January 10, 2002

Linking beta-catenin to androgen signaling pathway

Fajun Yang, Xiaoyu Li, Manju Sharma, Carl Y. Sasaki, Dan L. Longo, Bing Lim, and Zijie Sun

Dept. of Surgery & Genetics, Stanford University School of Medicine, Stanford, CA 94305-5328

Corresponding Author: zsun{at}stanford.edu

The androgen-signaling pathway is important for the growth and progression of prostate cancer cells. The growth-promoting effects of androgen on prostate cells are mediated mostly through the androgen receptor (AR). There is increasing evidence that transcription activation by AR is mediated through interaction with other co-factors. b-catenin plays a critical role in embryonic development and tumorigenesis through its effects on E-cadherin-mediated cell adhesion and Wnt-dependent signal transduction. Here, we demonstrate that a specific protein-protein interaction occurs between b-catenin and AR. Unlike the steroid hormone receptor coactivator 1 (SRC1), b-catenin showed a strong interaction with AR but not with other steroid hormone receptors such as PRb, ERa, and GR. The ligand binding domain of AR and the N-terminus combined with the first 6 armadillo repeats of b-catenin were shown to be necessary for the interaction. Through this specific interaction, b-catenin augments the ligand-dependent activity of AR in prostate cancer cells. Moreover, expression of E-cadherin in E-cadherin negative prostate cancer cells results in redistribution of the cytoplasmic b-catenin to the cell membrane and reduction of AR-mediated transcription. These data suggest that loss of E-cadherin can elevate the cellular levels of b-catenin in prostate cancer cells, which may directly contribute to invasiveness and a more malignant tumor phenotype by augmenting AR activity during prostate cancer progression.


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