This Article Full Text Full Text (PDF) Purchase Article View Shopping Cart Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Copyright Permission Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Maffini, M. V. Articles by Soto, A. M. Search for Related Content PubMed PubMed Citation Articles by Maffini, M. V. Articles by Soto, A. M.

Mechanism of Androgen Action on Cell Proliferation: AS3 Protein as a Mediator of Proliferative Arrest in the Rat Prostate

Department of Anatomy and Cellular Biology, Tufts University School of Medicine, Boston, Massachusetts 02111-1800

Address all correspondence and requests for reprints to: Ana M. Soto, Department of Anatomy and Cell Biology, Tufts University School of Medicine, 136 Harrison Avenue, Boston, Massachusetts 02111. E-mail: . ana.soto{at}tufts.edu

Androgens control the proliferation of their target cells first by increasing cell proliferation and later by inhibiting the proliferation of those same cells. Recently, we reported that the AS3 protein mediates the androgen-induced quiescence in androgen-target human cell lines. Our aims were to investigate the expression of the AS3 protein in the rat prostate in situ and in human cells in culture. Adult rats were separated into four groups (intact, castrated, castrated plus 3-d testosterone propionate replacement, and castrated plus 7-d testosterone propionate replacement). S9 cells expressing a tetracycline-regulated sense AS3 were also used. AS3 was expressed in the nuclei of over 90% of the epithelial cells and about 40% of the smooth muscle cells of the intact rat prostate. AS3 was not expressed in castrated rats or during the proliferative phase of androgen-induced regeneration. It was expressed in intact and castrated animals when the prostate has reached adult organ size. The AS3 protein was not expressed in cells that incorporate bromodeoxyuridine. These data suggest that AS3 is a mediator of the proliferative arrest in the normal rat prostate in situ and human prostate cell lines and that its expression is androgen-induced.

This article has been cited by other articles:

				B. Zhang, S. Jain, H. Song, M. Fu, R. O. Heuckeroth, J. M. Erlich, P. Y. Jay, and J. Milbrandt Mice lacking sister chromatid cohesion protein PDS5B exhibit developmental abnormalities reminiscent of Cornelia de Lange syndrome Development, September 1, 2007; 134(17): 3191 - 3201. [Abstract] [Full Text] [PDF]

				E. M. Reis, E. P.B. Ojopi, F. L. Alberto, P. Rahal, F. Tsukumo, U. M. Mancini, G. S. Guimaraes, G. M.A. Thompson, C. Camacho, E. Miracca, et al. Large-scale Transcriptome Analyses Reveal New Genetic Marker Candidates of Head, Neck, and Thyroid Cancer Cancer Res., March 1, 2005; 65(5): 1693 - 1699. [Abstract] [Full Text] [PDF]

				C. Sonnenschein and A. M. Soto Are Times a' Changin' in Carcinogenesis? Endocrinology, January 1, 2005; 146(1): 11 - 12. [Full Text] [PDF]

				S. A. Shain Exogenous Fibroblast Growth Factors Maintain Viability, Promote Proliferation, and Suppress GADD45{alpha} and GAS6 Transcript Content of Prostate Cancer Cells Genetically Modified to Lack Endogenous FGF-2 Mol. Cancer Res., November 1, 2004; 2(11): 653 - 661. [Abstract] [Full Text] [PDF]

				M. V. Maffini, A. M. Soto, J. M. Calabro, A. A. Ucci, and C. Sonnenschein The stroma as a crucial target in rat mammary gland carcinogenesis J. Cell Sci., March 15, 2004; 117(8): 1495 - 1502. [Abstract] [Full Text] [PDF]