Abstract
Nicotinamide (NAM) is a water-soluble form of Vitamin B3 (niacin) and a precursor of nicotinamide-adenine dinucleotide (NAD+) which regulates cellular energy metabolism. Except for its role in the production of adenosine triphosphate (ATP), NAD+ acts as a substrate for several enzymes including sirtuin 1 (SIRT1) and poly ADP-ribose polymerase 1 (PARP1). Notably, NAM is an inhibitor of both SIRT1 and PARP1. Accumulating evidence suggests that NAM plays a role in cancer prevention and therapy. Phase III clinical trials have confirmed its clinical efficacy for non-melanoma skin cancer chemoprevention or as an adjunct to radiotherapy against head and neck, laryngeal, and urinary bladder cancers. Evidence for other cancers has mostly been collected through preclinical research and, in its majority, is not yet evidence-based. NAM has potential as a safe, well-tolerated, and cost-effective agent to be used in cancer chemoprevention and therapy. However, more preclinical studies and clinical trials are needed to fully unravel its value.
Highlights
Cancer is a multistep process caused by an accumulation of molecular aberrations—activation of oncogenes, inhibition of tumor suppressor genes, epigenetic plasticity—that deregulate intracellular signaling pathways and drive cancer initiation and progression [1,2,3]
This review examines the role of nicotinamide (NAM) in cancer chemoprevention and therapy
NAM is a precursor of nicotinamide-adenine dinucleotide (NAD+), which takes part in several redox and non-redox reactions that regulate cellular energy metabolism (Figure 1) [38,39]
Summary
Cancer is a multistep process caused by an accumulation of molecular aberrations—activation of oncogenes, inhibition of tumor suppressor genes, epigenetic plasticity—that deregulate intracellular signaling pathways and drive cancer initiation and progression [1,2,3]. Normal tissues give rise to premalignant changes and, when the genetic alterations pile up to a higher number, the latter progress to malignancy (cancer) [1,2,3]. Through this process, cells gradually acquire traits that allow them to sustain uncontrolled proliferation, evade apoptosis, enhance angiogenesis, induce epithelial-mesenchymal transition (EMT), invade, and metastasize [4,5,6,7]. As cancer progresses, it accumulates genetic and epigenetic alterations becomes more heterogeneous The latter could be associated with resistance to chemotherapy or targeted therapy [33,34]. It first starts with a brief description of NAM basic principles and metabolism, continues with the existing evidence on its potential utility in chemoprevention, chemotherapy, and radiotherapy, and finishes with a discussion of the findings in addition to future perspectives
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
