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Originally published In Press as doi:10.1074/jbc.M202584200 on May 20, 2002

J. Biol. Chem., Vol. 277, Issue 31, 27793-27800, August 2, 2002
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New Human Breast Cancer Cells to Study Progesterone Receptor Isoform Ratio Effects and Ligand-independent Gene Regulation*

Britta M. JacobsenDagger §, Jennifer K. RicherDagger , Stephanie A. SchittoneDagger , and Kathryn B. HorwitzDagger ||

From the Departments of Dagger  Medicine and  Pathology and the || Molecular Biology Program, University of Colorado Health Sciences Center, Denver, Colorado 80262

All known progesterone target cells coexpress two functionally different progesterone receptor (PR) isoforms: 120-kDa B-receptors (PR-B) and N-terminally truncated, 94-kDa A-receptors (PR-A). Their ratio varies in normal and malignant tissues. In human breast cancer cells, homodimers of progesterone-occupied PR-A or PR-B regulate different gene subsets. To study PR homo- and heterodimers, we constructed breast cancer cell lines in which isoform expression is controlled by an inducible system. PR-negative cells or cells that stably express one or the other isoform were used to construct five sets of cells: (i) PR-negative control cells (Y iNull), (ii) inducible PR-A cells (Y iA), (iii) inducible PR-B cells (Y iB), (iv) stable PR-B plus inducible PR-A cells (B iA), and (v) stable PR-A plus inducible PR-B cells (A iB). Expression levels of each isoform and/or the PR-A/PR-B ratios could be tightly controlled by the dose of inducer as demonstrated by immunoblotting and transcription studies. Induced PRs underwent normal progestin-dependent phosphorylation and down-regulation and regulated exogenous promoters as well as endogenous gene expression. Transcription of exogenous promoters was dependent on the PR-A/PR-B ratio, whereas transcription of endogenous genes was more complex. Finally, we have described several genes that are regulated by induced PR-A even in the absence of ligand.

* This work was supported in part by National Institutes of Health Grants DK48238 and CA26869, Department of Defense Research Service Command Grant BC981225, and National Foundation for Cancer Research Grant 10COL3.The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

§ Supported by National Research Service Award postdoctoral fellowship CA90073 F32. To whom correspondence should be addressed: Dept. of Medicine/Endocrinology, University of Colorado School of Medicine, 4200 E. 9th Ave., Campus Box B151, Denver, CO 80262. Tel.: 303-315-8850; Fax: 303-315-4525; E-mail: Britta.Jacobsen@uchsc.edu.

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