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The adipocyte-derived hormone leptin has proliferative actions on androgen-resistant prostate cancer cells linking obesity to advanced stages of prostate cancer.

Hoda MR, Theil G, Mohammed N, Fischer K, Fornara P - J Oncol (2012)

Bottom Line: Background.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.

View Article: PubMed Central - PubMed

Affiliation: Clinic for Urology and Kidney Transplantation Centre, University Medical School of Halle/Wittenberg, Ernst-Grube-Strasse 40, 06120 Halle, Saale, Germany.

ABSTRACT
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.

No MeSH data available.


Related in: MedlinePlus

Leptin increases cell proliferation in androgen-resistant prostate cancer cell lines ((a); PC-3, (b); DU145) in a dose-dependent manner. Conversely, leptin's proliferative effect on androgen-sensitive cell line ((c); LNCaP) was much less pronounced. Cells were cultured in serum-free media for 24 hours (white bars) or 48 hours (black bars) in the presence or absence of leptin (0–100 ng/mL) and cell numbers were determined by a colorimetric XTT assay. Assays were performed at least five times and samples were run in triplicate. The data (means ± SEM) are reported as a percentage of results in untreated controls and asterisks or pound signs denote values significantly different from these cells at 24 and 48 hrs, respectively, (* or #P < 0.05; ** or ##P < 0.01; *** or ###P < 0.001 by ANOVA).
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fig1: Leptin increases cell proliferation in androgen-resistant prostate cancer cell lines ((a); PC-3, (b); DU145) in a dose-dependent manner. Conversely, leptin's proliferative effect on androgen-sensitive cell line ((c); LNCaP) was much less pronounced. Cells were cultured in serum-free media for 24 hours (white bars) or 48 hours (black bars) in the presence or absence of leptin (0–100 ng/mL) and cell numbers were determined by a colorimetric XTT assay. Assays were performed at least five times and samples were run in triplicate. The data (means ± SEM) are reported as a percentage of results in untreated controls and asterisks or pound signs denote values significantly different from these cells at 24 and 48 hrs, respectively, (* or #P < 0.05; ** or ##P < 0.01; *** or ###P < 0.001 by ANOVA).

Mentions: Leptin increased cell numbers in both androgen-resistant cell lines after 24 hrs and 48 hrs of incubation; whereas leptin's proliferative effect on androgen-sensitive cells was much less pronounced. As shown in Figures 1(a)–1(c), cell numbers were dose-dependently (5–100 ng/mL) increased at 24 and 48 hours after leptin treatment in DU145 and PC-3 cell lines when compared to cell numbers in serum-free control cultures. Maximal growth responses were observed after 48 h at a leptin concentration of 100 ng/mL: 161.2 ± 5.1% of control in DU145 cells (P < 0.001) and 182.7 ± 7.9% of control in PC-3 cells (P < 0.001). However, treatment of LNCaP cells with leptin (100 ng/mL) for up to 48 hours triggered only a small effect on cell proliferation (percent of control; 112.3 ± 6.1%; 100 ng/mL leptin; 48 hrs).


The adipocyte-derived hormone leptin has proliferative actions on androgen-resistant prostate cancer cells linking obesity to advanced stages of prostate cancer.

Hoda MR, Theil G, Mohammed N, Fischer K, Fornara P - J Oncol (2012)

Leptin increases cell proliferation in androgen-resistant prostate cancer cell lines ((a); PC-3, (b); DU145) in a dose-dependent manner. Conversely, leptin's proliferative effect on androgen-sensitive cell line ((c); LNCaP) was much less pronounced. Cells were cultured in serum-free media for 24 hours (white bars) or 48 hours (black bars) in the presence or absence of leptin (0–100 ng/mL) and cell numbers were determined by a colorimetric XTT assay. Assays were performed at least five times and samples were run in triplicate. The data (means ± SEM) are reported as a percentage of results in untreated controls and asterisks or pound signs denote values significantly different from these cells at 24 and 48 hrs, respectively, (* or #P < 0.05; ** or ##P < 0.01; *** or ###P < 0.001 by ANOVA).
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3368429&req=5

fig1: Leptin increases cell proliferation in androgen-resistant prostate cancer cell lines ((a); PC-3, (b); DU145) in a dose-dependent manner. Conversely, leptin's proliferative effect on androgen-sensitive cell line ((c); LNCaP) was much less pronounced. Cells were cultured in serum-free media for 24 hours (white bars) or 48 hours (black bars) in the presence or absence of leptin (0–100 ng/mL) and cell numbers were determined by a colorimetric XTT assay. Assays were performed at least five times and samples were run in triplicate. The data (means ± SEM) are reported as a percentage of results in untreated controls and asterisks or pound signs denote values significantly different from these cells at 24 and 48 hrs, respectively, (* or #P < 0.05; ** or ##P < 0.01; *** or ###P < 0.001 by ANOVA).
Mentions: Leptin increased cell numbers in both androgen-resistant cell lines after 24 hrs and 48 hrs of incubation; whereas leptin's proliferative effect on androgen-sensitive cells was much less pronounced. As shown in Figures 1(a)–1(c), cell numbers were dose-dependently (5–100 ng/mL) increased at 24 and 48 hours after leptin treatment in DU145 and PC-3 cell lines when compared to cell numbers in serum-free control cultures. Maximal growth responses were observed after 48 h at a leptin concentration of 100 ng/mL: 161.2 ± 5.1% of control in DU145 cells (P < 0.001) and 182.7 ± 7.9% of control in PC-3 cells (P < 0.001). However, treatment of LNCaP cells with leptin (100 ng/mL) for up to 48 hours triggered only a small effect on cell proliferation (percent of control; 112.3 ± 6.1%; 100 ng/mL leptin; 48 hrs).

Bottom Line: Background.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.

View Article: PubMed Central - PubMed

Affiliation: Clinic for Urology and Kidney Transplantation Centre, University Medical School of Halle/Wittenberg, Ernst-Grube-Strasse 40, 06120 Halle, Saale, Germany.

ABSTRACT
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.

No MeSH data available.


Related in: MedlinePlus