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烟酰胺腺嘌呤二核苷酸池增加通过抑制活性氧水平促进结肠癌进展。

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

机构信息

Department of Biochemistry and Department of Biomedical Sciences (BK21 Plus), Ajou University School of Medicine, Suwon, Korea.

Department of Gastroenterology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea.

出版信息

Cancer Sci. 2019 Feb;110(2):629-638. doi: 10.1111/cas.13886. Epub 2018 Dec 27.

DOI:10.1111/cas.13886
PMID:30457689
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6361564/
Abstract

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 FK866, 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.

摘要

烟酰胺腺嘌呤二核苷酸 (NAD) 有氧化型 (NAD ) 和还原型 (NADH) 两种存在形式。NAD 在癌症代谢中起着至关重要的作用，包括细胞信号转导、能量产生和氧化还原调节。然而，NAD(H) 池大小（NAD 和 NADH）是否可作为结肠癌进展的生物标志物仍不清楚。在这里，我们发现由于烟酰胺磷酸核糖转移酶（NAMPT）介导的 NAD 补救途径的激活，NAD(H) 池大小和 NAD/NADH 比值在结直肠癌细胞（CRC）进展过程中均增加。CRC 患者的腺瘤和腺癌组织中 NAMPT 表达上调。通过双光子激发荧光（TPEF）显微镜测量的 NADH 荧光强度在 CRC 细胞系、氧化偶氮甲烷/葡聚糖硫酸钠（AOM/DSS）诱导的 CRC 组织和 CRC 患者的肿瘤组织中持续增加。NAD(H) 池的增加抑制了过量活性氧（ROS）水平的积累，并且 NAMPT 的特异性抑制剂 FK866 处理通过增加 AOM/DSS 小鼠中的 ROS 水平降低了 CRC 结节的大小。总之，我们的研究结果表明，NAMPT 介导的 NAD(H) 池上调可保护癌细胞免受有害的氧化应激，并且通过 TPEF 显微镜检测 NADH 荧光可能是监测 CRC 进展的一种潜在方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5568/6361564/29feca84720e/CAS-110-629-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5568/6361564/54df2b08cffa/CAS-110-629-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5568/6361564/44e91f55b608/CAS-110-629-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5568/6361564/14a3b2d69578/CAS-110-629-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5568/6361564/6010dee18166/CAS-110-629-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5568/6361564/d1829853bddf/CAS-110-629-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5568/6361564/29feca84720e/CAS-110-629-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5568/6361564/54df2b08cffa/CAS-110-629-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5568/6361564/44e91f55b608/CAS-110-629-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5568/6361564/14a3b2d69578/CAS-110-629-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5568/6361564/6010dee18166/CAS-110-629-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5568/6361564/d1829853bddf/CAS-110-629-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5568/6361564/29feca84720e/CAS-110-629-g006.jpg

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