Background/aims: COX-2 (Cyclooxygenase-2) is the inducible isoform of cyclooxygenase in response to cytokines, mitogens, and growth factors and may induce carcinogenesis through the mechanisms of inhibiting apoptosis, increasing cell proliferation, and enhancing angiogenesis. This study aimed to clarify the relationship of COX-2 and p53, a well-known tumor suppressor gene, in gastric carcinoma.
Methodology: Immunohistochemical staining of nuclear p53 protein and cytoplasmic COX-2 protein were utilized on tumor tissue sections from 65 surgical specimens. Their correlation was further analyzed according to pathologic characteristics.
Results: There were 47% (16/34) of high COX-2 expression in the high p53 immunoreactivity group but only 19% (6/31) of high COX-2 expression in the low p53 immunoreactivity group. COX-2 overexpression significantly correlated with the accumulation of nuclear p53 protein in general (p = 0.035). Analysis based on different pathologic characteristics revealed that COX-2 correlates with p53 in subsets of advanced, cardiac, and H. pylori (-) gastric carcinomas (p = 0.027, 0.048, 0.036, respectively). But the relationship does not differ between Lauren's intestinal- and diffuse-type gastric carcinomas.
Conclusions: Our work provides evidence linking COX-2 and p53 in gastric carcinogenesis, but the mechanism how they interact to promote tumorigenesis remains to be elucidated.