Visfatin, Obesity, and Cancer

Abstract

Cancer represents an important public health concern. Overweight, obesity, and metabolic syndrome influence the risk and prognosis of several disease states including cancer. Metabolic changes related to visceral obesity could contribute to a dysfunctional adipose tissue provoking chronic subclinical inflammation, insulin resistance, and abnormal production of adipokines. Visfatin, found in the visceral adipose tissue, known also as nicotinamide phosphoribosyltransferase (Nampt) and pre-B-cell colony-enhancing factor (PBEF), acts as a multifaceted molecule with a triple action: a cytokine, a growth factor, and an enzyme. It exerts a pivotal role in a multitude of metabolic and stress responses and cellular bioenergetics, specifically nicotinamide adenine dinucleotide (NAD) synthesis. Visfatin/Nampt exhibits antiapoptotic, proliferative, pro-inflammatory, pro-angiogenic, and metastatic properties. The insulin-mimetic function of visfatin/Nampt remains a controversial issue. Circulating visfatin/Nampt is enhanced in many cancers, including obesity-associated malignancies. It is associated with bad prognosis and higher tumor stage and grade. Plasma visfatin/Nampt may be a novel risk factor as well as a surrogate clinical marker in cancer therapeutics. Moreover, pharmacologic neutralization of visfatin/Nampt employing agents that reduce its levels or downregulate signaling pathways downstream of visfatin/Nampt could be promising anticancer treatments. In this book chapter, we will particularly focus on both intracellular and extracellular visfatin/Nampt’s contribution to cancer pathophysiology as well as on the mechanisms underlying the connection between visfatin/Nampt and cancer. Further research is required in order to conclude whether visfatin/Nampt may be a therapeutic target in the pharmacological arsenal for cancer.