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Nitric oxide as a carcinogen: analysis by yeast functional assay of inactivating p53 mutations induced by nitric

J Murata1, M Tada, R D Iggo

  • 1Department of Neurosurgery, Hokkaido University School of Medicine, Sapporo, Japan.

Mutation Research
|November 14, 1997
PubMed

Insights

Nitric oxide and cytosine methylation induce mutations in the p53 tumor suppressor gene. Cytosine methylation is the primary driver of C:G-->T:A transitions at CpG sites, mimicking in vivo deamination.

Area of Science:

  • Molecular Biology
  • Genetics
  • Cancer Research

Background:

  • The p53 tumor suppressor gene is crucial for preventing cancer.
  • Mutations in p53 are common in many human cancers.
  • Nitric oxide and DNA methylation are implicated in carcinogenesis.

Purpose of the Study:

  • To investigate the mutagenic effects of nitric oxide and cytosine methylation on the p53 gene.
  • To elucidate the role of cytosine methylation in p53 mutations at CpG sites.

Main Methods:

  • Utilized a yeast functional assay to detect biologically relevant p53 mutations.
  • Treated p53 cDNA with a nitric oxide donor (sydnonimine).
  • Introduced cytosine methylation into p53 cDNA using PCR-mediated substitution or SssI CpG methylase.

Main Results:

  • Nitric oxide significantly increased C:G-->A:T transversions in a dose-dependent manner.
  • Cytosine methylation alone induced C:G-->T:A transitions.
  • Combined treatment with nitric oxide and methylation further increased mutation yield.

Conclusions:

  • Cytosine methylation is a key factor in C:G-->T:A transitions at CpG sites, supporting the deamination of 5-methylcytosine to thymine.
  • Nitric oxide primarily induces C:G-->A:T transversions.
  • These findings provide insights into p53 mutational mechanisms in cancer.

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