Expression of budding uninhibited by benzimidazoles-1 and mitotic arrest deficient-2 in endometrial carcinoma and its significance
Zhao, Q.; Bian, A.P.; Zhang, Y.; Qin, L.; Shi, H.R.; Su, K.
European Journal of Gynaecological Oncology 35(1): 44-47
2014
ISSN/ISBN: 0392-2936 PMID: 24654460 Document Number: 675909
The aim of this study was to explore the expression of budding uninhibited by benzimidazoles-1 (Bub1) and mitotic arrest deficient-2 (Mad2) in endometrial carcinoma and its significance. The expression of Bub 1 and Mad2 in 30 human normal endometrial tissues (group A), 30 complexly-hyperplastic endometrial tissues (group B), and 63 endometrial carcinoma tissues (group C) was observed using immunohistochemistry (the streptavidin-peroxidase method). The positive expression rates of Bub1 in groups A, B, and C were 86.67%, 56.67%, and 28.57%, respectively. The positive rate of Bub1 protein was correlated with the differentiation degree and clinical stage of endometrial carcinoma (p < 0.05) other than lymph node metastasis (p > 0.05): A higher differentiation degree and a more advanced stage of endometrial carcinoma indicated a higher positive rate of Bub1 protein. The positive rates of Mad2 protein in groups A, B, and C were 23.33%, 56.67%, and 85.71%, respectively. The positive rate of Mad2 protein was correlated with the differentiation degree of endometrial carcinoma (p < 0.05) other than its clinical stage and lymph node metastasis (p > 0.05): A lower differentiation degree indicated a higher positive rate of Mad2 protein. Bub1 and Mad2 proteins were negatively correlated in the endometrial carcinoma tissues (r = - 0.719, p < 0.001). Bub1 and Mad2 proteins interact with each other. They may play an important role in the initiation and development of endometrial carcinoma.