鞘脂激活蛋白C抑制LNCaP细胞雄激素受体降解的研究  

The study of saposin C down-regulates AR degradation in LNCaP cells

作　　者：任凯[1] 付慧[1] 陈鹏[1] 成凡[1] 茹晓荣[1] 郭慧芳[1] 

机构地区：[1]西安医学院生物化学教研室,西安710021

出　　处：《陕西医学杂志》2013年第11期1443-1445,共3页Shaanxi Medical Journal

基　　金：陕西省教育厅科研计划项目资助(12JK0711);西安医学院资助课题(11FZ18)

摘　　要：目的:探讨Saposin C对LNCaP细胞雄激素受体(AR)蛋白降解的影响。方法:通过转染实验,将Saposin C、TAT-Saposin C真核表达载体转染至LNCaP细胞,MTS检测Saposin C对LNCaP细胞增殖的影响,Western blot检测Saposin C对AR蛋白水平的影响及其在细胞中降解的调节作用。结果:Saposin C抑制LNCaP细胞AR蛋白的降解,上调胞内AR蛋白水平,促进LNCaP细胞增殖。结论:Saposin C增强AR蛋白的稳定性抑制其在细胞中的降解。Objective：To investigate the effect of Saposin C on Androgen Receptor protein degradation in LNCaP cells .Methods ：After transient transfection of the eukaryotic expression vectors containing Saposin C and TAT-Saposin C into LNCaP cells ,MTS was used to detect effects of Saposin C and TAT-Saposin C on proliferation of LNCaP cells .Western blot assay was used to investigate effects of Saposin C and TAT-Saposin C on AR protein levels .Results ：Saposin C and TAT-Saposin C could promote the proliferation of LNCaP cells .Its mechanism was that Saposin C and TAT-Saposin C up-regulated AR protein stability and restrained AR protein degradation .Conclu-sion：Saposin C could enhance AR protein levels and stability .

关 键 词：前列腺肿瘤 生物学 鞘脂激活蛋白 分析 @雄激素受体 

分 类 号：R34[医药卫生—基础医学]