TLR2及β-arrestin2在子宫内膜癌中的表达及关系的初步研究

目的:初步研究TLR2及β-arrestin 2在子宫内膜癌发生、发展及转移中的表达及关系。方法:(1)选取2005年11月至2011年9月北京大学人民医院的组织标本80例,其中正常子宫内膜20例,子宫内膜非典型增生20例,子宫内膜癌40例(其中复发转移癌20例)。采用免疫组化染色检测TLR2及β-arrestin 2的表达。(2)分别转染β-arrestin 2空白荧光质粒(GFP)、β-arrestin 2全长质粒(全长质粒过表达组)及β-arrestin 2干扰RNA质粒(β-arrestin 2-iRNA干扰组)至子宫内膜癌HEC-1B细胞,real-time PCR方法验证转染效果,同法测定各组总RNA中TLR2、MYD88、NF-κB的表达。结果:子宫内膜癌组织中TLR2、β-arrestin 2表达均显著高于正常内膜组织及非典型增生组织(P均0.01),TLR2与β-arrestin 2表达呈正相关(r=0.875,P0.01)。TLR2、MYD88、NF-κB在β-arrestin 2-iRNA干扰组中表达降低(P0.05),在全长质粒过表达组中表达增高(P0.05)。结论:β-arrestin 2可作为TLR2激动剂,激活TLR2途径的MyD88依赖型信号转导通路活化NF-κB。

The preliminary research on the relationship of the expression and regulation between TLR2 and beta-arrestin 2 in endometrial carcinoma.

Objective：Preliminary study of the expression and regulation between TLR2 （toll-like receptor） and beta-arrestin 2 in the process of occurrence, development and metastasis of endometrial carcinoma. Methods ： （ 1 ） 80 paraffin uterine specimens from Peking University People＇s hospital were collected from Nov. 2005 to Sep. 2011, including 20 cases of normal endometrium ,20 cases of endometrial atypical hyperplasia, and 40 cases with endometrial carcinoma, of which 20 cases with recurrence and metastasis. TLR2 and β-arrestin 2 in all cases were labeled with immunohistochemistry stain. （2）GFP plasmids, full-length and interferenced RNA （iRNA） plasmids were respectively transfeeted into endometrial HEC-1 B ceils. Real-time PCR was performed to verify transfection effects, and to test expression quantities of TLR2, MYD88, NF-κB in each group respectively. Results ：The expressions of TLR2 and beta-arrestin 2 in the endometrial carcinoma group were obviously higher than that in normal endometrium and atypical hyperplasia groups （ P〈0.01 ）. Expression levels of TLR2 and beta-arrestin 2 were positively correlated（r = 0. 875, P〈0.01 ）. Expressions of TLR2, MYD88, NF-κB in β-arrestin 2-iRNA interference group of HEC-1B cells decreased, yet that in full-length plasmid group increased（P〈0.05）. Conclusions： β-arrestin 2 can act as TLR2 agonist to activate TLR2 pathways,which can activate the MyD88 dependent signal transduction pathways and activate the NF-κB.