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Journal of Biomedicine and Biotechnology
Volume 2008, Article ID 163902, 8 pages
http://dx.doi.org/10.1155/2008/163902
Research Article

Differential Effects of Leptin on the Invasive Potential of Androgen-Dependent and -Independent Prostate Carcinoma Cells

1Department of Biochemistry, Louisiana State University Health Science Center, New Orleans, LA 70112, USA
2Department of Surgery, University of South Alabama Medical Center, Mobile, AL 36617, USA
3Department of Pathology and Genetics, Louisiana State University Health Science Center, New Orleans, LA 70112, USA
4Stanley S. Scott Cancer Center, Louisiana State University Health Science Center, New Orleans, LA 70112, USA
5Department of Pediatrics, University of South Alabama Medical Center, Mobile, AL 36617, USA
6Brady Urological Institute, The Johns Hopkins Medical Institutions, Baltimore, MD 21287, USA
7Department of Obstetrics and Gynecology, Louisiana State University Health Science Center, New Orleans, LA 70112, USA

Received 25 October 2007; Revised 10 February 2008; Accepted 8 April 2008

Academic Editor: Yan Luo

Copyright © 2008 Dayanand D. Deo et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Obesity has been linked with an increased risk of prostate cancer. The formation of toxic free oxygen radicals has been implicated in obesity mediated disease processes. Leptin is one of the major cytokines produced by adipocytes and controls body weight homeostasis through food intake and energy expenditure. The rationale of the study was to determine the impact of leptin on the metastatic potential of androgen-sensitive (LNCaP) cells as well as androgen-insensitive (PC-3 and DU-145) cells. At a concentration of 200_nm, LNCaP cells showed a significant increase (20% above control; ) in cellular proliferation without any effect on androgen-insensitive cells. Furthermore, exposure to leptin caused a significant ( to ) dose-dependent decrease in migration and invasion of PC3 and Du-145 prostate carcinoma cell lines. At the molecular level, exposure of androgen-independent prostate cancer cells to leptin stimulates the phosphorylation of MAPK at early time point as well as the transcription factor STAT3, suggesting the activation of the intracellular signaling cascade upon leptin binding to its cognate receptor. Taken together, these results suggest that leptin mediates the invasive potential of prostate carcinoma cells, and that this effect is dependent on their androgen sensitivity.