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目的探讨β-arrestin 2在不同子宫内膜组织中的表达及其与血管生成之间的关系。方法选取2002年9月至2010年12月间北京大学人民医院的组织标本75例,其中正常子宫内膜19例,子宫内膜非典型增生20例,子宫内膜癌24例,复发转癌12例。对其进行CD34及β-arrestin 2免疫组化染色。分别转染β-arrestin 2空白荧光质粒、全长质粒及干扰RNA质粒入子宫内膜癌HEC-1A细胞,ELISA方法测定各组上清中VEGF的表达量。结果子宫内膜癌组微血管密度(MVD)值明显高于正常内膜组及非典型增生组(P<0.05);子宫内膜癌组中β-arrestin 2表达明显高于其他各组(P<0.001);MVD与β-arrestin 2表达呈正相关(r=0.557,P<0.001);过表达β-arrestin 2可促进VEGF分泌。结论β-arrestin 2可促进子宫内膜癌细胞分泌VEGF,从而促进新生血管的形成,导致子宫内膜癌的进展。
Objective To investigate the expression of β-arrestin 2 in different endometrial tissues and its relationship with angiogenesis. Methods Seventy-five specimens of Peking University People’s Hospital from September 2002 to December 2010 were selected, including 19 cases of normal endometrium, 20 cases of endometrial atypical hyperplasia, 24 cases of endometrial carcinoma, 12 cases of recurrent carcinoma example. CD34 and beta-arrestin 2 immunohistochemical staining. The transfected β-arrestin 2 blank fluorescent plasmids, full-length plasmids and interfering RNA plasmids into endometrial carcinoma cell line HEC-1A were respectively transfected into HEC-1A cells. The expression of VEGF in supernatant of each group was measured by ELISA. Results The microvessel density (MVD) in endometrial carcinoma was significantly higher than that in normal endometrial and atypical hyperplasia (P <0.05). The expression of β-arrestin 2 in endometrial carcinoma was significantly higher than that in other groups (P < 0.001). MVD was positively correlated with β-arrestin 2 expression (r = 0.557, P <0.001). Overexpression of β-arrestin 2 promoted VEGF secretion. Conclusion β-arrestin 2 can promote the secretion of VEGF in endometrial cancer cells, so as to promote the formation of new blood vessels and lead to the progression of endometrial cancer.