Expression Of CYP4501B1and COMT Protein In Human Endometrial Hyperplasia

Objective: Endometrial hyperplasia is a common disease in gynecologywhich has a certain tendency to carcinogenesis. It is of great significance tomake a correct diagnosis in time and give treatment in preventing progressionof lesion. Endometrial hyperplasia is divided into simple hyperplasia, complexhyperplasia and atypical hyperplasia. Atypical hyperplasia has tendency tocancer, which belongs to the precancerous lesion. Chronic estrogenstimulation may be the main reason of endometrial hyperplasia withoutantagonist from progesterone. Cytochrome P4501B1(CYP1B1) involves inestrogen metabolism, which is expressed in a variety of malignant tumortissues with high frequency and high value (includes breast, colon, esophagus,endometrium, ovary, skin and lymph nodes), while in the normal tissue with alow expression or non. Catechol-O-methyltransferase (COMT) can converttoxic estrogen metabolites into non-toxic substances which can be removedfrom the body. The aim of this study was to investigate the expression ofCYP1B1and COMT in endometrial hyperplasia, to analyse the association ofthe both with the development of endometrial hyperplasia.Methods: The expression of CYP1B1and COMT were examined bywestern blot in22normal endometrium,13simple&complex hyperplasia and11atypical hyperplasia, then to compare the differences. The bands weregotten by computer Infrared Imagination and were analysed. The ration of thegray value of protein to the internal parameter was acted as the expression ofprotein respectively.Statistical analysis was performed using SPSS13.0software package. Thenormality of protein expression level was analysed by the test of normality.Comparison of three groups was performed by the One-Way ANOVA.Comparison of two groups by SNK if the groups have a significant difference. P<0.05was considered as significance.Results:1CYP1B1protein expression in endometrial hyperplasia tissuesThe expressions of CYP1B1were2.375±0.421in normal tissue,2.674±0.337in simple&complex hyperplasia，2.911±0.452in atypical hyperplasia. Thedifferences were significant among three groups (P=0.003). And according toSNK multiple comparison test, there was no significant difference betweennormal endometrial tissues and simple&complex hyperplasia, and betweensimple&complex hyperplasia and atypical hyperplasia. While there wassignificant difference between normal endometrial tissues and atypicalhyperplasia (P<0.05).2S-COMT protein expression in endometrial hyperplasia tissuesThe expressions of S-COMT were1.604±0.397in normal endometrial tissues,1.489±0.373in simple&complex hyperplasia，1.165±0.514in atypicalhyperplasia. The differences were significant among three groups (P=0.025).And according to SNK multiple comparison test, there was no significantdifference between normal endometrial tissues and simple&complexhyperplasia. There was significant difference between normal endometrialtissues and atypical hyperplasia, and between simple&complex hyperplasiaand atypical hyperplasia (P<0.05).3M-COMT protein expression in endometrial hyperplasia tissuesThe expression of M-COMT were2.094±0.469in normal endometrial tissues,1.853±0.432in simple&complex hyperplasia,1.692±0.428in atypicalhyperplasia. There were no significant differences among three groups (P=0.051).Conclusion:1The expression of CYP1B1was high in endometrial hyperplasiatissues, low in the normal tissues, indicating that the change of CYP1B1isassociated with the endometrial hyperplasia development;2The expression of CYP1B1was high in atypical hyperplasia tissues,low in the normal tissues, indicating that CYP1B1may be the prognostic factor of endometrial precancerous lesion.3The expression of S-COMT was lower in endometrial hyperplasiatissues than in normal endometrial tissues, indicating that S-COMT may be aprotective factor in endometrial hyperplasia. The expression of M-COMT waslow in atypical hyperplasia tissues, but its effect to endometrial precancerouslesion is difficult to determine.4CYP1B1and S-COMT may become the new therapy target ofendometrial hyperplasia.