Obesity is a complex chronic disorder that can result in a number of metabolic and endocrine disturbances and may thus account for the disparity seen in epidemiologic studies investigating the association between obesity and prostate cancer. Although the association between dietary factors and the occurrence of prostate cancer has been studied extensively, there is yet to be a published study on the relationship between diet and disease progression among prostate cancer patients. Circulating levels of most adipokines are positively correlated with obesity and exert a variety of biologic effects on prostate cancer cells modulating a variety of cellular processes. This would suggest that the presence of obesity may promote the progression of established prostate cancer rather than being a risk factor for the development of prostate cancer; however, a direct link has yet to be established. Recognizing adipose tissue as a metabolically active endocrine organ and identifying tumor promoting adipokines would support such an association.

To better understand the effects of increased dietary fat in prostate cancer, we used the prostate-specific PTEN conditional knockout mouse model to show that consumption of a high-fat diet (HFD) promoted prostate-specific cancer progression and decreased survival. Molecular analysis identified elevated levels of leptin as a likely molecule involved in driving tumor progression. In this study we provide data from in vitro experiments show that leptin promoted invasiveness, motility and adhesion of PC3, human prostate cancer cells. Together, our findings show that increased levels of leptin, induced by dietary fat, contributes to promote prostate cancer progression by upregulating STAT3 signal cascades.

Citation Format: Marco A. De Velasco, Yutaka Yamamoto, Yuji Hatanaka, Yurie Kura, Naomi Ando, Emiko Fukushima, Masahiro Nozawa, Nobutaka Shimizu, Kazuhiro Yoshimura, Kazuhiro Yoshikawa, Kazuto Nishio, Hirotsugu Uemura. Leptin contributes to prostate cancer progression. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 3688. doi:10.1158/1538-7445.AM2013-3688

©2013 American Association for Cancer Research
2013