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Expression of type 2 nitric oxide synthase and p21 in oral squamous cell carcinoma

P A Brennan1, M Palacios-Callender, T Umar

  • 1Maxillofacial Unit, Poole Hospital, Dorset, UK.

International Journal of Oral and Maxillofacial Surgery
|July 10, 2002
PubMed

Insights

Nitric oxide synthase-2 (NOS2) activity is linked to its expression in oral cancer, but not to p21 accumulation. High nitric oxide (NO) levels are unlikely to directly induce apoptosis in these cancers.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Nitric oxide (NO) plays a complex role in tumor biology, with research often focusing on nitric oxide synthase-2 (NOS2).
  • The tumor suppressor gene p53 typically promotes apoptosis via the p21 pathway in response to high NO concentrations, safeguarding against DNA damage.
  • In cancer cells with mutant p53, direct p53-dependent apoptosis is less likely, though p53-independent p21 expression and apoptosis can occur at elevated NO levels.

Purpose of the Study:

  • To investigate the direct association between NOS2 and p21 expression in oral squamous cell carcinoma.
  • To determine if NO concentrations in oral cancer are sufficient to induce p53-independent apoptosis via p21 accumulation.

Main Methods:

  • Immunohistochemistry was used to assess NOS2 and p21 expression in 56 oral squamous cell carcinoma cases.
  • NOS2 activity was quantified using citrulline assays in selected samples.

Main Results:

  • A significant correlation was found between NOS2 immunohistochemical expression and its enzymatic activity (P<0.001).
  • No significant relationship was observed between NOS2 expression and p21 expression (P=0.76).
  • Measured NO concentrations in oral cancer tissues were insufficient to directly induce p21 accumulation and apoptosis.

Conclusions:

  • NOS2 activity is directly related to its expression in oral squamous cell carcinoma.
  • The NO levels typically found in oral cancer do not appear sufficient to trigger direct p53-independent apoptosis through p21.
  • Pharmacological inhibition of NO production presents a potential therapeutic strategy for oral cancer, warranting further investigation.

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