Abstract
ABSTRACTObesity is defined as a chronic and excessive growth of adipose tissue. It has been associated with a high risk for development and progression of obesity-associated malignancies, while adipokines may mediate this association. Adiponectin is an adipose tissue-derived adipokines, with significant anti-diabetic, anti-inflammatory, anti-atherosclerotic and anti-proliferative properties. Plasma adiponectin levels are decreased in obese individuals, and this feature is closely correlated with development of several metabolic, immunological and neoplastic diseases. Recent studies have shown that prostate cancer patients have lower serum adiponectin levels and decreased expression of adiponectin receptors in tumor tissues, which suggests plasma adiponectin level is a risk factor for prostate cancer. Furthermore, exogenous adiponectin has exhibited therapeutic potential in animal models. In this review, we focus on the potential role of adiponectin and the underlying mechanism of adiponectin in the development and progression of prostate cancer. Exploring the signaling pathways linking adiponectin with tumorigenesis might provide a potential target for therapy.
Highlights
Prostate cancer (PC) recently became the second most prevalent cancer afflicting men, and the fifth leading cause of cancer related death throughout the World [1, 2]
Adiponectin and prostate cancer Adiposity has been consistently associated with an increased risk of progression of PC, but APN is inversely related to the degree of adiposity
APN can attenuate the adverse effects of leptin and inhibit LNCaP and PC3 proliferation via modulation of p53 and bcl-2 expression [41], the balance of leptin and APN may be important in driving obesity-related PC progression
Summary
Prostate cancer (PC) recently became the second most prevalent cancer afflicting men, and the fifth leading cause of cancer related death throughout the World [1, 2]. Adiponectin and prostate cancer Adiposity has been consistently associated with an increased risk of progression of PC, but APN is inversely related to the degree of adiposity. It seems that plasma APN should be reduced in PC patients. A study of 300 Greek men by Michalakis et al [16] revealed a significantly reduced risk of PC with higher plasma APN concentrations. Liao Q [26] performed a meta-analysis of numerous studies and concluded that patients with PC markedly had lower APN levels than controls, they found that decreased concentration of APN was associated with a significantly greater risk of PC. APN induced cell cycle arrest of prostatic epithelial and stromal cell lines through
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