作者: Chenpeng Zhang , Jinlu Tong , Gang Huang
DOI: 10.1371/JOURNAL.PONE.0069963
关键词:
摘要: A number of cancers show increased expression Nicotinamide phosphoribosyl transferase (Nampt). However, the mechanism through which Nampt is upregulated unclear. In our study, we found that Nampt-specific chemical inhibitor FK866 significantly inhibited cell survival and reduced nicotinamide adenine dinucleotide (NAD) levels in LoVo SW480 lines. Bioinformatics analyses suggested miR-26b targets mRNA. We identified as a new target demonstrated inhibits at protein mRNA by binding to 3′-UTR. Moreover, was down regulated cancer tissues relative adjacent normal 18 colorectal patients. statistically significant inverse correlation between observed samples from patients 5 lines (HT-29, SW480, SW1116, LoVo, HCT116). addition, over strongly invasion, an effect partially abrogated addition NAD. conclusion, this study NAD-salvaging biosynthesis pathway involving might play role survival. MiR-26b may serve tumor suppressor targeting Nampt.