Increased levels of NAD+ boost glycolysis and allow for the quick proliferation of cancer cells.
During these reactions, NAD+ is destroyed. For tumor cells, the high turnover rate of NAD+ is because of the high activity of ADP-ribosylation by PARPs (poly(ADP-ribose) polymerases). Critically low levels of NAD+ in cells causes metabolic collapse and death of the cell. Because of this, the tumor cells need to replenish lost NAD+ molecules via ingestion or biosynthesis.
Biosynthesis of NAD+ involves two important enzymes; Nampt and Nmnat. Nampt converts nicotinamide (NAM) and 5-phosphoribose-1-pyrophosphate (PRPP) to nicotinamide mononucleotide (NMN). From this, Nmnat creates NAD by moving a moiety of an adenylyl from ATP to NMN. Nampt is often overexpressed in several types of cancer, such as colorectal, ovarian, breast, and gastric tumors.
It has been found that levels of Nampt are upregulated in some cancers, implicating that it has a role in maintaining NAD+ levels in the cell. The inhibition of Nampt is associated with lethal reductions in NAD+ levels. However, Nampt is also needed in healthy cells, meaning any use in therapeutic settings needs to be thoroughly evaluated for deleterious side effects before use can be widespread.
https://www.news-medical.net/life-sciences/NAD2b-Metabolism-in-Cancer-and-Cancer-Therapies.aspx