Nicotinamide Phosphoribosyltransferase in Malignancy: A Review
Author(s) -
Rodney E. Shackelford,
Kim Mayhall,
N. M. Maxwell,
Emad Kandil,
Domenico Coppola
Publication year - 2013
Publication title -
genes and cancer
Language(s) - Uncategorized
Resource type - Journals
SCImago Journal Rank - 1.883
H-Index - 71
eISSN - 1947-6027
pISSN - 1947-6019
DOI - 10.1177/1947601913507576
Subject(s) - nicotinamide phosphoribosyltransferase , nad+ kinase , malignancy , carcinogenesis , nicotinamide adenine dinucleotide , cancer research , medicine , nicotinamide , cancer , limiting , oncology , bioinformatics , enzyme , chemistry , biology , biochemistry , mechanical engineering , engineering
Nicotinamide phosphoribosyltransferase (Nampt) catalyzes the rate-limiting step of nicotinamide adenine dinucleotide (NAD) synthesis. Both intracellular and extracellular Nampt (iNampt and eNampt) levels are increased in several human malignancies and some studies demonstrate increased iNampt in more aggressive/invasive tumors and in tumor metastases. Several different molecular targets have been identified that promote carcinogenesis following iNampt overexpression, including SirT1, CtBP, and PARP-1. Additionally, eNampt is elevated in several human cancers and is often associated with a higher tumor stage and worse prognoses. Here we review the roles of Nampt in malignancy, some of the known mechanisms by which it promotes carcinogenesis, and discuss the possibility of employing Nampt inhibitors in cancer treatment.
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