Expression Of COX-2 And NF-κB In Endometrial Carcinoma And Their Correlation

Objectives: To detect the expression of cyclooxygenase-2 (COX-2) and nuclear factor-kappaB (NF- κ B) and their relationship with clinical -pathologic parameters in endometrial cancer, thereby investigate the role of COX-2 and NF-κ B in the carcinogensis and development of endometrial carcinoma, and evaluate the role of NF- κ B on COX-2 expression in the endometrial carcinoma.Methods: The endometrial tissue specimens were obtained from 10 cases with proliferative phase, 10 cases with secretory phase, 20 cases with atypical proliferative phase and 45 cases with endometrial carcinoma. Immunohistochemistry (with SP method) was utilized to measure levels of expression of COX-2 and NF- κ B-P65 in the endometrial tissue specimens. Results: Expression of COX-2 was detected in tissues of endometrial carcinoma, atypical proliferative phase and normal endometrium. The positive expression of COX-2 in tissues of endometrial carcinoma was higher (77.8%) significantly than normal and atypical proliferative phase endometrium(15%,50% P<0.01).The positive expression of COX-2 in tissues of atypical proliferative phase endometrium was higher (50%) significantly than proliferative phase and secretory phase endometrium (10%,20% P<0.05),while there was no significant difference between the latter two groups. COX-2 positivity increased from mild dysplasia (22.2%) to moderateand severe dysplasia (72.7%) in tissues of atypical proliferative phase endometrium. The percentage of COX-2 positivity was higher (89.3%) in well differentiated endometrial carcinoma tissues than that in moderately and poorly differentiated tissues (58.8% P<0.05). There was no correlation between COX-2 expression with any other clinicalpathologic parameters such as myometrial invasion, lymph node status or FIGO stage. All of the normal endometrium and endometrial hyperplasia tissues were scored as NF-k B-P65 positive, but NF- k B-P65 expression was lower(82.2%) in carcinoma tissues. The percentage of NF- k B-P65 positivity was higher(92.9%) in well differentiated endometrial carcinoma tissues than that in moderately and poorly differentiated tissues (64.7% PO.05). NF- k. B-P65 expression did not correlated with myometrial invasion, lymph node status or FIGO stage. Though the expression of NF- k. B-P65 decreased, there was a positive correlation between COX-2 and NF- k B expression in endometrial carcinoma tissues (r=0.509 PO.01) .Conclusion: Expression of COX-2 showed an increasing tendency from normal endometrium to endometrial hyperplasia to endometrial carcinoma, and higher significantly in well differentiated endometrial carcinoma tissues than that in moderately and poorly differentiated tissues, which suggested up-regulation of COX-2 may be an early event in the tumorigenesis of endometrial carcinoma. Though NF- k B expression was lower in carcinoma tissues, there was a positive correlation between COX-2 and NF- k B expression in endometrial carcinoma tissues. This implied that NF- k B may play an important role in COX-2 induction in the endometrial carcinoma. Our dates suggests that COX-2 plays important role in the carcinogensis anddevelopment of endometrial carcinoma, and NF- k B may be involved in COX-2 induction. However, further study should be performed to confirm this conclusion and elucidate the precise role of NF- k B and COX-2 in the initiation and promotion of endometrial carcinoma.