Cancer Research CTRC-AACR San Antonio Breast Cancer Symposium AACR Conference on Molecular Diagnostics - 2008
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[Cancer Research 63, 958-964, March 1, 2003]
© 2003 American Association for Cancer Research

Endocrinology

Peroxisome Proliferator-activated Receptor {gamma} Agonists Induce Proteasome-dependent Degradation of Cyclin D1 and Estrogen Receptor {alpha} in MCF-7 Breast Cancer Cells1

Chunhua Qin, Robert Burghardt, Roger Smith, Mark Wormke, Jessica Stewart and Stephen Safe2

Departments of Veterinary Physiology and Pharmacology [C. Q., M. W., J. S., S. S.], Veterinary Anatomy and Public Health [R. B.], and Veterinary Pathobiology [R. S.], Texas A&M University, College Station, Texas, and Institute of Biosciences and Technology, The Texas A&M University System Health Science Center, Houston, Texas 77843-4466 [S. S.]

Treatment of MCF-7 cells with the peroxisome proliferator-activated receptor (PPAR) {gamma} agonists ciglitazone or 15-deoxy-{Delta}12,14-prostaglandin J2 resulted in a concentration- and time-dependent decrease of cyclin D1 and estrogen receptor (ER) {alpha} proteins, and this was accompanied by decreased cell proliferation and G1-G0->S-phase progression. Down-regulation of cyclin D1 and ER{alpha} by PPAR{gamma} agonists was inhibited in cells cotreated with the proteasome inhibitors MG132 and PSII, but not in cells cotreated with the protease inhibitors calpain II and calpeptin. Moreover, after treatment of MCF-7 cells with 15-deoxy-{Delta}12,14-prostaglandin J2 and immunoprecipitation with cyclin D1 or ER{alpha} antibodies, there was enhanced formation of ubiquitinated cyclin D1 and ER{alpha} bands. Thus, PPAR{gamma}-induced inhibition of breast cancer cell growth is due, in part, to proteasome-dependent degradation of cyclin D1 (and ER{alpha}), and this pathway may be important for other cancer cell lines.




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