CD38 Inhibits Prostate Cancer Metabolism and Proliferation by Reducing Cellular NAD Pools.

Tumor cells require increased rates of cell metabolism to generate the macromolecules necessary to sustain proliferation. They rely heavily on NAD as a cofactor for multiple metabolic enzymes in anabolic and catabolic reactions. NAD also serves as a substrate for PARPs, sirtuins, and cyclic ADP-ribose synthases.

Nicotinamide phosphoribosyl transferase (Nampt) is required for de novo lipogenesis in tumor cells.

Tumor cells have increased metabolic requirements to maintain rapid growth. In particular, a highly lipogenic phenotype is a hallmark of many tumor types, including prostate. Cancer cells also have increased turnover of nicotinamide adenine dinucleotide (NAD(+)), a coenzyme involved in multiple metabolic pathways.