Background:Because obesity may be a risk factor for prostate cancer, we investigated proliferative effects of adipocytes-derived hormone leptin on human prostate cancer cells and assessed the role of mitogen-activated protein kinase (MAPK) signaling pathway in mediating these actions.
Material and Methods:Three human prostate cancer cell lines were treated with increasing doses of recombinant leptin. Cell growth was measured under serum-free conditions using a spectrophotometric assay. Further, Western blotting was applied to detect the phosphorylation of an ERK1/2, and a specific inhibitor of MAPK (PD98059; 40 μM) was used.
Results:In both androgen-resistant cell lines DU145 and PC-3, cell growth was dose-dependently increased by leptin after 24 hrs and 48 hrs of incubation, whereas leptin's proliferative effects on androgen-sensitive cell line LNCaP was less pronounced. Further, leptin caused dose-dependent ERK1/2 phosphorylation in both androgen-resistant cell lines, and pretreatment of these cells with PD98059 inhibited these responses.
Conclusions: Leptin may be a potential link between obesity and risk of progression of prostate cancer. Thus, studies on leptin and obesity association to prostate cancer should differentiate patients according to androgen sensitivity.
Written by:
Hoda MR, Theil G, Mohammed N, Fischer K, Fornara P. Are you the author?
Clinic for Urology and Kidney Transplantation Centre, University Medical School of Halle/Wittenberg, Ernst-Grube-Strasse 40, 06120 Halle, Saale, Germany.
Reference: J Oncol. 2012;2012:280386.
doi: 10.1155/2012/280386
PubMed Abstract
PMID: 22690216
UroToday.com Investigative Urology Section
