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J. Biol. Chem. 277 (13): 11336-11344

© 2002 by The American Society for Biochemistry and Molecular Biology, Inc.

Linking β-Catenin to Androgen-signaling Pathway*

Fajun Yang{ddagger}, Xiaoyu Li§, Manju Sharma{ddagger}, Carl Y. Sasaki, Dan L. Longo, Bing Lim§, , and Zijie Sun{ddagger}||

From the {ddagger}Department of Surgery and Department of Genetics, Stanford University School of Medicine, Stanford, California 94305-5328, the §Division of Hematology/Oncology, Department of Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts 02115, and the Laboratory of Immunology, NIA, National Institutes of Health, Baltimore, Maryland 21224

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Abstract: 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 cofactors. β-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 β-catenin and AR. Unlike the steroid hormone receptor coactivator 1 (SRC1), β-catenin showed a strong interaction with AR but not with other steroid hormone receptors such as estrogen receptor α, progesterone receptor β, and glucocorticoid receptor. The ligand binding domain of AR and the NH2terminus combined with the first six armadillo repeats of β-catenin were shown to be necessary for the interaction. Through this specific interaction, β-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 β-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 β-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.

Received for publication December 14, 2001. Revision received January 8, 2002.

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