OBJECTIVE: To investigate the effects of leptin, full-length adiponectin (fAd) and globular adiponectin (gAd), alone and in combination, on LNCaP and PC3 prostate cancer cell proliferation, and on the expression of p53 and bcl-2 gene expression. MATERIALS AND METHODS: LNCaP and PC3 prostate cancer cells were cultured and treated with the following: 0-100 nM leptin; 0-100 nM fAd +/- 100 nM leptin; 0-100 nM gAd +/- 100 nM leptin. Proliferation assays and quantitative reverse transcriptase-polymerase chain reaction for p53 tumour-suppressor gene and bcl-2 oncogene expression were performed on treated samples. RESULTS: Co-incubation of PC3 cells with 100 nM leptin and 1 or 100 nM fAd significantly decreased cell proliferation to approximately half of basal (P < 0.001); there was no significant effect in LNCaP cells. Leptin-induced inhibition of p53 expression in LNCaP cells was rescued by fAd. Leptin and fAd dose-dependently potentiated p53 expression in PC3 cells (P < 0.001); leptin and gAd also increased p53 expression (P < 0.05 and P < 0.001). fAd and gAd had no effect on bcl-2 expression in the presence of leptin in LNCaP cells. In PC3 cells, bcl-2 expression was inhibited to negligible levels in the presence of leptin. CONCLUSIONS: Leptin and adiponectin interact, resulting in the inhibition of prostate cancer cell proliferation, particularly in PC3 cells, via modulation of p53 and bcl-2 expression. Our findings support the notion that high leptin and low adiponectin levels may be important in driving obesity-related prostate cancer progression.
OBJECTIVE: To investigate the effects of leptin, full-length adiponectin (fAd) and globular adiponectin (gAd), alone and in combination, on LNCaP and PC3 prostate cancer cell proliferation, and on the expression of p53 and bcl-2 gene expression. MATERIALS AND METHODS: LNCaP and PC3 prostate cancer cells were cultured and treated with the following: 0-100 nM leptin; 0-100 nM fAd +/- 100 nM leptin; 0-100 nM gAd +/- 100 nM leptin. Proliferation assays and quantitative reverse transcriptase-polymerase chain reaction for p53 tumour-suppressor gene and bcl-2 oncogene expression were performed on treated samples. RESULTS: Co-incubation of PC3 cells with 100 nM leptin and 1 or 100 nM fAd significantly decreased cell proliferation to approximately half of basal (P < 0.001); there was no significant effect in LNCaP cells. Leptin-induced inhibition of p53 expression in LNCaP cells was rescued by fAd. Leptin and fAd dose-dependently potentiated p53 expression in PC3 cells (P < 0.001); leptin and gAd also increased p53 expression (P < 0.05 and P < 0.001). fAd and gAd had no effect on bcl-2 expression in the presence of leptin in LNCaP cells. In PC3 cells, bcl-2 expression was inhibited to negligible levels in the presence of leptin. CONCLUSIONS:Leptin and adiponectin interact, resulting in the inhibition of prostate cancer cell proliferation, particularly in PC3 cells, via modulation of p53 and bcl-2 expression. Our findings support the notion that high leptin and low adiponectin levels may be important in driving obesity-related prostate cancer progression.
Authors: Anya J Burton; Kate M Tilling; Jeff M Holly; Freddie C Hamdy; Mari-Anne E Rowlands; Jenny L Donovan; Richard M Martin Journal: Int J Mol Epidemiol Genet Date: 2010-07-25
Authors: Edward A Medina; Xiaoyu Shi; Marcia H Grayson; Donna P Ankerst; Carolina B Livi; Maria V Medina; Ian M Thompson; Robin J Leach Journal: Cancer Epidemiol Biomarkers Prev Date: 2013-12-02 Impact factor: 4.254