Differential Effects of Leptin on the Invasive Potential of Androgen-Dependent and -Independent Prostate Carcinoma Cells. (22nd June 2008)

• Record Type: Journal Article
• Authors: Deo, Dayanand D.; Rao, Ashwin P.; Bose, Saideep S.; Ouhtit, Allal; Baliga, Surendra B.; Rao, Shilpa A.; Trock, Bruce J.; Thouta, Rajesh; Raj, Madhwa HG; Rao, Prakash N.
• Other Names: Luo Yan Academic Editor.
• Is Part Of: Journal of biomedicine and biotechnology. Volume 2008(2008)
• Publication Date: 2008-06-22
• Subjects: Medicine -- Periodicals; Biology -- Periodicals; Biotechnology -- Periodicals; Medicine; Biology; Biotechnology; Médecine; Biologie; Biotechnologie; Biology; Biotechnology; Medicine; Biotechnology; Biomedicine; Electronic journals; Periodical; Periodicals; Electronic journals; 610
• DOI: 10.1155/2008/163902
• Languages: English
• ISSNs: 1110-7243

Abstract

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; P < .0001 ) in cellular proliferation without any effect on androgen-insensitive cells. Furthermore, exposure to leptin caused a significant (P < .01 to P < .0001 ) 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.