Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2007) 14 P136

ECE2007 Poster Presentations (1) (659 abstracts)

Leptin and adiponectin interact in regulating prostate cancer cell growth

Tina Mistry 1 , Janet Digby 1 , Ken Desai 2 & Harpal Randeva 1

1University of Warwick Medical School, Coventry, United Kingdom; 2University Hospital Coventry and Warwickshire, Coventry, United Kingdom.

Introduction: Leptin and adiponectin have opposing properties and are implicated as molecular mediators between obesity and (aggressive) prostate cancer. Adiponectin, circulates inversely proportional to visceral fat accumulation, and has demonstrated anti-proliferative effects in prostate cancer cells; circulating leptin levels increase with visceral fat accumulation and has shown mitogenic effects. We propose that adiponectin and leptin interact in prostate cancer cell growth regulation.

Materials and Methods: We studied the effect of full-length (fAd) and globular (gAd) adiponectin (0.01 nM–100 nM) ± 100 nM leptin on LNCaP and PC3 prostate cancer cell proliferation. p53 tumour suppressor and bcl-2 oncogene expression was measured using quantitative RT-PCR.

Results: LNCaP: co-incubation of fAd with leptin resulted in decreased cell proliferation; fAd alone had little effect. gAd alone slightly increased proliferation and had little effect when co-incubated with leptin. fAd alone increased p53 mRNA expression and rescued leptin-induced inhibition of p53 expression; both fAd and gAd alone increased bcl-2 expression, but reduced expression to below basal when co-incubated with leptin. PC3: fAd decreased proliferation at 100nM, but reduced proliferation to half of basal when co-incubated with leptin; gAd alone increased proliferation but reduced proliferation to basal when co-incubated with leptin. Both fAd and gAd demonstrated significant dose-dependent increases in p53 mRNA expression when co-incubated with leptin; both fAd and gAd reduced bcl-2 expression to negligible levels despite the addition of leptin.

Conclusion: We show an interaction between adiponectin and leptin in the regulation of prostate cancer cell proliferation through modulation of p53 and bcl-2 expression; this is most marked in the advanced PC3 cell line. Concurrent hyperleptinaemia and hypoadiponectinaemia in obese patients may modulate prostate cancer progression, and serum leptin:adiponectin ratio could represent a new prognostic marker; increasing circulating fAd in these patients may be a novel treatment for this disease.

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