This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted 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 Briehl, M. M. Articles by Miesfeld, R. L. Search for Related Content PubMed PubMed Citation Articles by Briehl, M. M. Articles by Miesfeld, R. L.

Transcriptional Analyses of Steroid-Regulated Gene Networks

Departments of Biochemistry, Molecular and Cellular Biology and Arizona Cancer Center, University of Arizona Tucson, Arizona 85721

Address requests for reprints to: Dr. Roger Miesfeld, Arizona Cancer Center, University of Arizona, Tucson, Arizona 85724.

Abstract

It has been proposed that cell-specific responses to steroid action are the result of coordinate expression of steroid gene networks. Using three different cell systems, we have performed transcriptional analyses to determine if the observed hormoneinduced alterations in gene expression are consistent with a limited number of potential target genes in any one cell type. Our results indicate that greater than 95% of the transcripts in dexamethasonetreated rat hepatoma (HTC), or mouse lymphoma (WEHI7) cells, are similar to the mRNAs in untreated cells based on subtraction hybridization. In addition, we find that although the castration-induced expression of androgen-regulated transcripts in the rat ventral prostate (RVP) is significantly different between normal and castrated rats (19%), the majority of these mRNAs are accounted for by the over abundance of sulfated glycoprotein-2 sequences. Specifically, analysis of an RVP subtracted cDNA library revealed that sulfated glycoprotein-2 mRNA masked the presence of less abundant differentially expressed sequences, confirming that the actual size of the RVP androgen gene network is small. We conclude that steroid-mediated changes in transcription accurately reflect the expression of a few cell-specific target genes, and thus support the model of steroid gene networks. The potential to characterize key elements which determine both the time course and magnitude of cell-specific hormone responses is discussed.

FOOTNOTES

This research was supported by grants from the NIH (GM-40738) and the American Cancer Society (NP-702) (to R. M.), and NIH Postdoctoral Cancer Biology Training Grant CA-09213 (to M.B.)

^* Scholar of the Leukemia Society of America.

Received for publication July 26, 1989. Revision received October 31, 1989. Accepted for publication November 5, 1989.

This article has been cited by other articles:

				E. B. Thompson and B. H. Johnson Regulation of a Distinctive Set of Genes in Glucocorticoid-evoked Apoptosis in CEM Human Lymphoid Cells Recent Prog. Horm. Res., January 1, 2003; 58(1): 175 - 197. [Abstract] [Full Text] [PDF]

				R. D. Medh Microarray-Based Expression Profiling of Normal and Malignant Immune Cells Endocr. Rev., June 1, 2002; 23(3): 393 - 400. [Abstract] [Full Text] [PDF]

				S. Greenstein, K. Ghias, N. L. Krett, and S. T. Rosen Mechanisms of Glucocorticoid-mediated Apoptosis in Hematological Malignancies Clin. Cancer Res., June 1, 2002; 8(6): 1681 - 1694. [Abstract] [Full Text] [PDF]

				D. C. Whitacre, S. Chauhan, T. Davis, D. Gordon, A. E. Cress, and R. L. Miesfeld Androgen Induction of in Vitro Prostate Cell Differentiation Cell Growth Differ., January 1, 2002; 13(1): 1 - 11. [Abstract] [Full Text] [PDF]