Prostate cancer (PCa) is the most common type of cancer among men over 60 years old. The aggressiveness and mortality of PCa can be correlated with obesity. Adipose tissue-derived cytokines such as adiponectin may explain the correlation between PCa and obesity. Since the correlation between adiponectin and aggressive PCa is still not fully evaluated, we aimed to investigate the probable role of adiponectin in PCa. Adiponectin is considered as a link between obesity, insulin resistance and diabetes. On the other hand, adiponectin is a key mediator of systemic insulin sensitivity and glucose homeostasis. Moreover, low level of adiponectin is associated with inflammation and angiogenesis. These processes could promote tumor growth. Special effects of adiponectin are mediated via adenosine monophosphate-activated protein kinase (AMPK). AMPK activation inhibits growth of androgen-independent and androgen-sensitive PCa cell lines. Moreover, c-Jun N-terminal protein kinase (JNK) and Signal transducer and activator of transcription 3 (STAT3) signaling pathway are known as adiponectin’s mediators on the metabolic syndrome and cancer. Furthermore, adiponectin acts as a tumor suppressor gene via inhibition of Epithelial-to-mesenchymal Transition (EMT) of PCa cells, but it is down regulated through hypermethylation of promoter gene in PCa cells. Therefore, according to the results of these studies, decreased concentration of adiponectin was associated with increased risk of PCa. It seems that hypoadiponectinemia may act as a promising biomarker for detection and diagnosis of PCa.