Ovarian cancer (OC) is one of the most fatal gynecological neoplasms. Meta-analyses have shown that the relationship between body mass index (BMI) and ovarian cancer incidence was detected in some types of ovarian cancer. Chronic inflammation and excessive accumulation of free fatty acids are key adipose tissue-derived factors initiating cancer development. Cancer cells transform adipose-derived stem cells into cancer-associated adipocytes, which produce adipokines and interleukins. It was revealed that adipokines exert a pleiotropic role in ovarian cancer pathogenesis. Chemerin presents both pro-cancer and anti-cancer action in ovarian cancer development. Chemerin induces angiogenesis and increases programmed death ligand-1 (PD-L1) expression, leading to enhanced proliferation and migration of OC cells. Apelin impacts cancer cell migration and acts as a mitogenic factor. Moreover, apelin exerts influence on lipid uptake into cancer cells and accelerates fatty acid oxidation, which provides energy for cancer cells. Visfatin induces matrix metallopeptidase 2 (MMP2) expression involved in extracellular matrix degradation and suppresses claudin 3 and 4 expression. Visfatin also induces a shift to anaerobic glucose metabolism and influences poly-ADP ribose polymerase (PARP). Resistin induces MMP2 and vascular endothelial growth factor (VEGF) expression and contributes to cisplatin-resistance development. A substantial body of evidence indicates that antagonists of adipokines mitigate OC progression, and adipokines are gaining gradual recognition as a potential therapeutic aim in ovarian cancer targeted therapy.
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