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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 ^,

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. Rustgi^1,2,3*

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), and there was a concomitant increase in lipogenic gene expression as a downstream effector of PPAR. Importantly, Parvin-β suppressed breast cancer growth in vivo, with associated decreased proliferation. These data suggest that Parvin-β might influence breast cancer progression.

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* 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

Published ahead of print on 12 November 2007.

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

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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.

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