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Molecular and Cellular Biology, January 2008, p. 687-704, Vol. 28, No. 2
0270-7306/08/$08.00+0     doi:10.1128/MCB.01617-06
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Parvin-β Inhibits Breast Cancer Tumorigenicity and Promotes CDK9-Mediated Peroxisome Proliferator-Activated Receptor Gamma 1 Phosphorylation{triangledown} ,{dagger}

Cameron N. Johnstone,1,2 Perry S. Mongroo,1,2,5 A. Sophie Rich,1 Michael Schupp,4 Mark J. Bowser,1,2 Andrew S. deLemos,1,2 John W. Tobias,7 Yingqiu Liu,8 Gregory E. Hannigan,5,6 and Anil K. Rustgi1,2,3*

Division of Gastroenterology, Department of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104,1 Abramson Cancer Center, University of Pennsylvania, Philadelphia, Pennsylvania 19104,2 Department of Genetics, University of Pennsylvania, Philadelphia, Pennsylvania 19104,3 Division of Endocrinology, Diabetes, and Metabolism, Department of Medicine, and Institute of Diabetes, Obesity and Metabolism, University of Pennsylvania, Philadelphia, Pennsylvania 19104,4 Cancer Research Program, Hospital for Sick Children, Toronto, Ontario M5G 1X8, Canada,5 Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Ontario M5G 1X8, Canada,6 Penn Bioinformatics Core, Center for Bioinformatics, University of Pennsylvania, Philadelphia, Pennsylvania 19104,7 Division of Hematology/Oncology, Department of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 191048

Received 29 August 2006/ Returned for modification 26 September 2006/ Accepted 27 October 2007

Parvin-β is a focal adhesion protein downregulated in human breast cancer cells. Loss of Parvin-β contributes to increased integrin-linked kinase activity, cell-matrix adhesion, and invasion through the extracellular matrix in vitro. The effect of ectopic Parvin-β expression on the transcriptional profile of MDA-MB-231 breast cancer cells, which normally do not express Parvin-β, was evaluated. Particular emphasis was placed upon propagating MDA-MB-231 breast cancer cells in three-dimensional culture matrices. Interestingly, Parvin-β reexpression in MDA-MB-231 cells increased the mRNA expression, serine 82 phosphorylation (mediated by CDK9), and activity of the nuclear hormone receptor peroxisome proliferator-activated receptor gamma (PPAR{gamma}), and there was a concomitant increase in lipogenic gene expression as a downstream effector of PPAR{gamma}. Importantly, Parvin-β suppressed breast cancer growth in vivo, with associated decreased proliferation. These data suggest that Parvin-β might influence breast cancer progression.

* Corresponding author. Mailing address: Departments of Medicine and Genetics, Abramson Cancer Center, University of Pennsylvania, 600 Clinical Research Building, 415 Curie Blvd., Philadelphia, PA 19104. Phone: (215) 898-0154. Fax: (215) 573-2024. E-mail: anil2{at}mail.med.upenn.edu

{triangledown} Published ahead of print on 12 November 2007.

{dagger} Supplemental material for this article may be found at http://mcb.asm.org/.

Molecular and Cellular Biology, January 2008, p. 687-704, Vol. 28, No. 2
0270-7306/08/$08.00+0     doi:10.1128/MCB.01617-06
Copyright © 2008, American Society for Microbiology. All Rights Reserved.





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