Sequential expression of inducible nitric oxide synthase and cyclooxygenase-2 during DMBA-induced hamster buccal

Soo-A Kim1, Sang-Gun Ahn, Do Kyung Kim

  • 1Oral Biology Research Institute, BK 21 Project, Chosun University School of Dentistry, Gwangju, Korea.

In Vivo (Athens, Greece)
|November 5, 2004
PubMed
Abstract

Insights

Inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) expression increases during oral carcinogenesis. Their combined action may promote tumor growth, highlighting their role in oral cancer development.

Area of Science:

  • Oncology
  • Molecular Biology
  • Oral Pathology

Background:

  • Inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) are known to be expressed in oral premalignant and malignant lesions.
  • The interaction and co-expression patterns of iNOS and COX-2 during oral carcinogenesis remain incompletely understood.

Purpose of the Study:

  • To investigate the expression levels of iNOS and COX-2 throughout the process of hamster buccal pouch (HBP) carcinogenesis.
  • To elucidate the potential cooperative role of iNOS and COX-2 in oral tumor progression.

Main Methods:

  • Immunohistochemical analysis was employed to assess iNOS and COX-2 expression.
  • The study examined normal mucosa, dysplastic lesions, and squamous cell carcinoma (SCC) at various differentiation stages.
  • Hamster buccal pouch carcinogenesis was induced using 7,12-dimethylbenz[a]anthracene (DMBA).

Main Results:

  • Both iNOS and COX-2 expression showed a gradual increase from normal tissue to dysplastic lesions and further to invasive SCC.
  • Squamous cell carcinoma (SCC) exhibited the highest mean expression levels for both iNOS and COX-2.
  • Statistically significant differences in iNOS and COX-2 expression were observed between normal tissues and dysplastic/carcinomatous lesions.

Conclusions:

  • The findings suggest that iNOS may enhance tumor growth by cooperating with COX-2.
  • Elevated expression of iNOS and COX-2 is implicated as a contributing factor in oral carcinogenesis.
  • Targeting the iNOS-COX-2 pathway could offer potential therapeutic strategies for oral cancer.

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