Nitric Oxide and Cancer Development

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  • Floyd Robert A.
    Oklahoma Medical Research Foundation Department of Biochemistry and Molecular Biology, University of Oklahoma Health Sciences Center
  • Kotake Yashige
    Oklahoma Medical Research Foundation
  • Towner Rheal A.
    Oklahoma Medical Research Foundation
  • Guo We-Xing
    Oklahoma Medical Research Foundation
  • Nakae Dai
    Tokyo Metropolitan Institute of Public Health Tokyo University of Agriculture
  • Konishi Yoichi
    International Federation of Societies of Toxicologic Pathologists

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The role of nitric oxide (NO) in cancer development has become a very active research area. This review presents an overview of many studies that implicate an important role of NO in the development of cancer. These include results in experimental models as well as many observations made on NO and inducible nitric oxide synthase (iNOS) in human cancers. Our survey of the literature has allowed us to conclude that in general large levels of NO will kill cancer cells but paradoxically at intermediate to lower levels NO prevents cancer cell apoptosis and enhances tumor growth. This basic tenet has been demonstrated in many experimental models. The mechanistic basis of how intermediate levels of NO mediate tumor development is an active area of research and is the subject of this review. NO mediated S-nitrosylation of key enzymes and regulatory proteins plays a critical role. Key proteins S-nitrosylated which enhance tumor development include several caspases involved in apoptosis, PTEN the tumor suppressor protein, Bcl-2 the mitochondrial protein which protects from apoptosis, OGG1 the DNA repair protein and methionine adenosyl transferase the liver protein which synthesizes adenosylmethionine. The S-nitrosylation of these proteins enhances DNA mutations, prevents cancer cell apoptosis and enhances oncogenic cell growth.

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