| Objective: Colorectal cancer is one of the common cancers in clinical medicine, and it has an increasing morbidity in our country. The pathogenesis is unclear now. This study was designed to investigate the mechanism of COX-2 and Bcl-2 in the origin and development of colorectal carcinoma by observing the expressions of COX-2 and Bcl-2 as well as their correlations with the bionomics of colorectal carcinoma.Methods: The expressions of COX-2 and Bcl-2 were determined by immunohistochemical staining with COX-2 and Bcl-2 monoclone antibody in 78 surgical specimens and endoscopic biopsy of colorectal carcinoma , 21 colorectal adenomas and 13 normal mucosal tissues. The results were graded by four scales: negative(-), slightly positive(+), moderately positive(++), intense positive(+++) by summing staining cells. The expressions of COX-2 and Bcl-2 in carcinoma, adenoma, and normal tissue were analyzed statistically by X~2 test and their relationships with the bionomics of colorectal carcinoma by Spearman test.Results:(1)The positive rate of COX-2 in colorectal carcinoma was 78.21%, which was markedly higher than that in colorectal adenomas (52.38%) and normal mucosal tissues (7.69%) (P<0.05). The positive rate of Bcl-2 in colorectal carcinoma, colorectal adenoma and normal tissue was 80.8% , 85.7%, and 38.5%, respectively. There was significant difference between normal tissue and colorectal carcinoma and colorectal adenoma (P<0.05). The positive rate of Bcl-2 in colorectal adenoma was higher than that in colorectal adenoma, but there was no statistical difference between them(P>0.05).(2) The expression of COX-2 was significantly correlated with lymph node metastasis, Duke's stage, differentiation of tumor (P<0.05). The rate of COX-2 expression in well-differentiated and moderately-differentiated group of colorectal carcinoma was 70.37%, and in poorly-differentiated and no-differentiated group was 95.83%. The expression of COX-2 was as high as 92.11% in colorectal carcinoma with lymph node metastasis, which was significantly higher than that without lymph node metastasis(65%)(P<0.05). The expressions of COX-2 in Duke's C and D stage were 94.44%, respectively, which were significantly higher than those in A and B stage (64.29%). No significant correlation was noted between COX-2 expression and sex, histologic type(P>0.05). The expression of Bcl-2 in carcinoma showes significant correlation with lymph node metastasis and Duke's stage (P< 0.05). The expression of Bcl-2 was as high as 90% in colorectal carcinoma without lymph node metastasis, which was significantly higher than that with lymph node metastasis(71.05%)(P<0.05).The expressions of Bcl-2 in Duke's A and B stage were 92.86%, which were significantly higher than those in C and D stage (66.67%). There was no significant correlation between Bcl-2 expression and sex, histologic type and differentiation of tumor(P>0.05).(3)There was a significant positive correlation between the expressions of COX-2 and Bcl-2 (r=0.294 ,P<0.05).Conclusions:(1) The positive rates of COX-2 in colorectal carcinoma was obviously higher than that in colorectal adenoma and in normal mucosal tissue.(2)The expression of COX-2 was significantly correlated with lymph node metastasis, Duke's stage, and differentiation of tumor. No significant correlation was noted between COX-2 expression and sex and histology of tumor.(3)The positive rates of Bcl-2 in colorectal carcinoma and colorectal adenomas were obviously higher than that in normal mucosal tissue.(4) The expression of Bcl-2 was significantly correlated with lymph node metastasis and Duke's stage. No significant correlation was noted between Bcl-2 expression and sex, histology and differentiation of tumor.(5) It is suggested that COX-2 may elicit cancerogenesis by up-regulation of Bcl-2 and inhibition of cell apoptosis. |
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