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COX-2 Expression gradually increased during DMBA-induced Hamster Buccal Pouch Carcinogenesis

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±èÁ¤¼® ( Kim Jeong-Seok ) - Á¶¼±´ëÇб³ Ä¡°ú´ëÇÐ ±¸°­º´¸®Çб³½Ç
À±Á¤ÈÆ (  ) - Á¶¼±´ëÇб³
¾È»ó°Ç (  ) - Á¶¼±´ëÇб³
±è¼ö¾Æ (  ) - Á¶¼±´ëÇб³ Ä¡°ú´ëÇÐ º´¸®Çб³½Ç

Abstract


Cyclooxygenase-2 (COX-2) is an inducible enzyme that is not found in normal conditions, but is induced by a variety of pathophysiologic conditions of tissues by growth factors, inflammatory stimuli, oncogenes and tumor promoters. COX-2 is upregulated in a number of epithelial cancers, including in oral premalignant and malignant lesions. The mode of action of COX-2 in carcinogenesis may include mutiple mechanisms that may be acting at different stages of malignant disease. In this study, the expression of COX-2 protein was assessed quantitatively and qualitatively by immunohistochemistry during DMBA-induced hamster buccal pouch carcinogenesis. The immunoreactivity for COX-2 protein increased as the tissue passed from hyperplasia to dysplasia and SCC. The highest mean expression was SCC at 14 week. The differences between COX-2 expression in the normal and that the dysplastic and carcinomatous lesions was statistically significant. In addition, the mean values of COX-2 expression in the stromal cells increased gradually during malignant progression. The results suggest that increased COX-2 expression may be associated with the chemically induced carcinogenic progression of hamster buccal pouch model. The gradual increasing COX-2 expression detected during the progressive manner toward more malignant lesions shows that the COX-2 protein can have an important role in both the early and the later stages of multistep oral carcinogenesis.

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COX-2;DMBA;Hamster buccal pouch carcinogenesis

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