Background: Although it is known that iNOS and COX-2 are abundantly expressed in oral premalignant and malignant lesions, respectively, the interaction between iNOS and COX-2 has not been extensively studied. The purpose of this study was to examine the alteration of the iNOS and COX-2 expression level during hamster buccal pouch (HBP) carcinogenesis.
Materials and methods: The expression of both iNOS and COX-2 on normal, dysplastic mucosa and squamous cell carcinoma (SCC) from different differentiation stages in 7, 12-dimethylbenz[a]anthracene (DMBA)-induced HBP carcinogenesis was examined using immunohistochemical analysis.
Results: The mean values of both iNOS and COX-2 expression increased gradually from control to dysplastic lesions and more to invasive SCC. The highest mean expression was SCC. The differences between both iNOS and COX-2 expression in the normal and that in the dysplastic and carcinoma lesions were statistically significant.
Conclusion: The results suggest that iNOS can enhance its ability to promote tumor growth in cooperation with COX-2. The expression of iNOS and COX-2 may be one of the factors that contribute to oral carcinogenesis.