The Androgen Receptor Can Promote Beta-Catenin Nuclear Translocation Independently of Adenomatous Polyposis Coli
Mulholland, David, Cheng, Helen, Reid, Kimberly, Rennie, Paul S., & Nelson, Colleen C. (2002) The Androgen Receptor Can Promote Beta-Catenin Nuclear Translocation Independently of Adenomatous Polyposis Coli. Journal of Biological Chemistry, 277(20), pp. 17933-17943.
We provide evidence that the androgen receptor (AR) can promote nuclear translocation of -catenin in LNCaP and PC3 prostate cancer cells. Using AR-expressing cells (LNCaP) and non-AR-expressing cells (PC3) we showed by time course cell fractionation that the AR can shuttle -catenin into the nucleus when exposed to exogenous androgen. Cells exposed to the synthetic androgen, R1881, show distinct, punctate, nuclear co-localization of the AR and -catenin. We further showed that the AR does not interact with adenomatous polyposis coli or glycogen synthase kinase-3 and, therefore, conclude that androgen-mediated transport of -catenin occurs through a distinct pathway. The minimal necessary components of the AR and -catenin required for binding nuclear accumulation of -catenin nuclear import appears to be the DNA/ligand binding regions and the Armadillo repeats of -catenin. We also employed a novel DNA binding assay to illustrate that -catenin has the capacity to bind to the probasin promoter in an AR-dependent manner. The physiological relevance of AR-mediated transport of -catenin and binding to an AR promoter appeared to be a substantial increase in AR transcriptional reporter activity. AR-mediated import represents a novel mode of nuclear accumulation of -catenin.
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|Item Type:||Journal Article|
|Additional Information:||Articles free to read on journal website after 12 months|
|Divisions:||Past > QUT Faculties & Divisions > Faculty of Science and Technology|
|Copyright Owner:||Copyright 2002 American Society for Biochemistry and Molecular Biology|
|Deposited On:||19 Oct 2007 00:00|
|Last Modified:||04 Feb 2015 06:05|
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