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Nitric oxide synthase 2 mRNA expression in relation to p53 and adenomatous polyposis coli mutations in primary

Karin Fransén1, Jan Dimberg, Anna Osterström

  • 1Department of Biomedicine and Surgery, Division of Cell Biology, Faculty of Health Sciences, Linköping University, S-581 85 Linköping, Sweden.

Surgery
|April 6, 2002
PubMed
Abstract

Insights

Nitric oxide synthase 2 (NOS2) is upregulated in colorectal tumors, but not due to p53 or APC gene mutations. This suggests other mechanisms drive NOS2 expression in colorectal cancer progression.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Inducible nitric oxide synthase 2 (NOS2) is upregulated in various cancers, suggesting a role in tumorigenesis.
  • The regulation of NOS2 in colorectal carcinomas is not well understood.
  • In vitro studies suggest p53 accumulation downregulates NOS2, and promoter analysis indicates potential regulation by the adenomatous polyposis coli (APC)/beta-catenin pathway.

Purpose of the Study:

  • To investigate the expression and regulation of NOS2 in colorectal carcinomas.
  • To determine the relationship between NOS2 expression and mutations in p53, APC, and beta-catenin genes.

Main Methods:

  • NOS2 mRNA expression was quantified using reverse transcriptase/real-time polymerase chain reaction in 59 colorectal carcinomas.
  • NOS2 protein presence and localization were assessed via Western blot and immunohistochemistry.
  • Mutations in p53, APC, beta-catenin, and loss of heterozygosity in the NOS2 gene region were analyzed.

Main Results:

  • NOS2 mRNA and protein expression were significantly elevated in colorectal tumors compared to normal tissue.
  • Immunohistochemistry showed extensive NOS2 staining in tumor epithelial cells.
  • Increased NOS2 mRNA expression correlated with earlier Dukes' stages (A and B) but not with p53/APC mutations or loss of heterozygosity.

Conclusions:

  • Inactivating mutations in the p53 and APC pathways do not explain the increased NOS2 expression in colorectal tumors.
  • The findings suggest alternative regulatory mechanisms for NOS2 in colorectal carcinogenesis.

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