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Nicotinamide adenine dinucleotide ( NAD ) exists in an oxidized form (NAD + ) and a reduced form (NADH).  NAD  +  plays crucial roles in cancer metabolism, including in cellular signaling, energy production and redox regulation. However, it remains unclear whether  NAD (H) pool size ( NAD  +  and  NADH ) could be used as biomarker for colon cancer progression. Here, we showed that the  NAD (H) pool size and  NAD  + / NADH  ratio both increased during colorectal cancer ( CRC ) progression due to activation of the  NAD  +  salvage pathway mediated by nicotinamide phosphoribosyltransferase (NAMPT). The  NAMPT  expression was upregulated in adenoma and adenocarcinoma tissues from  CRC  patients. The  NADH  fluorescence intensity measured by two‐photon excitation fluorescence ( TPEF ) microscopy was consistently increased in  CRC  cell lines, azoxymethane/dextran sodium sulfate (AOM/DSS)‐induced  CRC  tissues and tumor tissues from  CRC  patients. The increases in the  NAD (H) pool inhibited the accumulation of excessive reactive oxygen species ( ROS)  levels and  FK 866, a specific inhibitor of  NAMPT , treatment decreased the  CRC  nodule size by increasing  ROS  levels in  AOM / DSS  mice. Collectively, our results suggest that  NAMPT ‐mediated upregulation of the  NAD (H) pool protects cancer cells against detrimental oxidative stress and that detecting  NADH  fluorescence by  TPEF  microscopy could be a potential method for monitoring  CRC  progression.

Increased nicotinamide adenine dinucleotide pool promotes colon cancer progression by suppressing reactive oxygen species level