PARP inhibitors are a cancer treatment.
"Continuous replenishment of NAD
promotes the proliferation
and survival of fast-dividing cancer
cells because elevated NAD
levels enhance glycolysis via glyceraldehyde 3-phosphate dehydrogenase (GAPDH) and lactate dehydrogenase (LDH) that require NAD
as a co-enzyme (12, 13).
"Recently, several studies have indicated that NAD metabolism is involved in cancer development and progression and is considered a promising therapeutic target in cancer treatment. In this review, we summarize the roles of NAD metabolism in cancer pathogenesis."
"Overexpression of Nampt is frequently observed in several types of malignant tumors, including, colorectal, ovarian, breast, gastric, thyroid, prostate cancers, gliomas, and malignant lymphomas (29
). Increased NAD levels accompanied by Nampt overexpression sustain rapid cellular proliferation and promote cancer cell survival against anti-cancer cell reagents. In particular, elevated NAD levels boost glycolysis through glyceraldehyde 3-phosphate dehydrogenase (GAPDH) and lactate dehydrogenase (LDH) that require NAD as a co-enzyme and enhance anaerobic glycolysis (12
A well-known oncogene, c-MYC was reported to regulate Nampt expression in cancer cells (49
). c-MYC transcriptionally regulates the metabolic reprogramming of cancer cells by enhancing glucose uptake, glycolysis, and lactate production, the increase in Nampt expression by c-MYC may lead to the Warburg effects (50
). Several microRNAs regulate Nampt levels and promote cancer cell proliferation. miR26b reportedly suppresses Nampt expression by binding to the 3'-UTR in the Nampt gene. In colorectal cancer cells, miR26b is down regulated, leading to the overexpression of Nampt."