血管紧张素II2型受体——肿瘤细胞凋亡诱导因子  

AT2R:A apoptosis inducer for cancer cells

作　　者：段世超[1] 费扬[1] 黄植[1] 杜红延[1] 李红卫[1] 李明[1] 

机构地区：[1]南方医科大学生物技术学院,广东广州510515

出　　处：《分子诊断与治疗杂志》2012年第4期279-283,共5页Journal of Molecular Diagnostics and Therapy

基　　金：国家高技术研究发展计划(863计划)(2012AA020205);国家自然科学基金(81072113)

摘　　要：血管紧张素Ⅱ(angiotensinⅡ,AngⅡ)是由8个氨基酸组成的线性小肽,是肾素-血管紧张素系统(renin-angiotensin system,RAS)的主要效应因子。血管紧张素Ⅱ1型(angiotensinⅡ1receptor,AT1R)和血管紧张素Ⅱ2型受体(angiotensinⅡ 2 receptor,AT2R)分别是AngⅡ作用的靶细胞的表面特异性G蛋白偶联1型和2型受体。AngⅡ通过上述2种受体参与调节血管舒缩、水盐平衡、细胞增殖、炎性反应、细胞凋亡等生物学功能。目前对AT1R的研究较多,在多种组织和器官中AT1R几乎介导了AngⅡ所有已知的生物学功能,但还不十分明确AT2R功能。随着对AngⅡ受体与肿瘤关系认识的深入,AT2R与肿瘤之间的联系也越来越受到重视。近年来AT2R诱导细胞凋亡的作用在肿瘤细胞中也有所发现,这提示AT2R可能作为肿瘤凋亡诱导因子来发挥作用,并有望成为肿瘤治疗的新靶点。Angiotensin Ⅱ, a linear small peptide,which is composed of eight amino acids, is the main effectors of renin-angiotensin systen（Renin-angiotensin system, RAS）. Ang Ⅱ, a main biopolypeptide of the RAS, has important pathophysiologic in effects participating in cardiac hypertrophy, vascular cell proliferation, inflammation and tissue remodeling through G-protein-coupled receptors, AT1R and AT2R. Numerous studies reported that almost all Ang Ⅱ effects mainly are mediated via the AT1R not AT2R, and little function of AT2R has been known. Along with more and more research on the relationship between the receptors of Ang II and tumor, AT2R gained more attention from researchers. It has been found that AT2R overexpression in some tumor cells could inhibit cells proliferation and induce apoptosis, which indicated that AT2R could be regarded as an apoptosis inducer and a promising novel target for tumor gene therapy.

关 键 词：血管紧张素Ⅱ AT2R 肿瘤 凋亡 

分 类 号：R730.2[医药卫生—肿瘤]