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作 者:卞倩[1]
机构地区:[1]江苏省疾病预防控制中心,江苏南京210009
出 处:《江苏预防医学》2008年第4期8-10,共3页Jiangsu Journal of Preventive Medicine
摘 要:目的:探讨RASSF1A肿瘤抑制效应的可能机制及其与细胞凋亡和MOAP-1蛋白表达的关系。方法:利用细胞培养及转染技术,将RASSF1A和/或MOAP-1质粒转染到H1299细胞中,用TRAIL诱导瞬时转染细胞H1299或稳定转染细胞HCT116,以及Hela细胞,用免疫共沉淀、Western Blot和激光共聚焦等方法检测RASSF1A与MOAP-1的相关性。结果:RASSF1A与MOAP-1共表达时,可发生蛋白-蛋白交互作用;RASSF1A可改变MOAP-1的表达模式,使其从线粒体进入微管,呈现与RASSF1A相似的表达形态;当RASSF1A高表达时,MOAP-1的蛋白表达亦相应增高,进而促进细胞凋亡的发生。结论:RASSF1A可通过与MOAP-1的蛋白交互作用,促进MOAP-1的表达,激活Bax介导的凋亡通路的信号传导,发挥其抑癌效应。Objective.. To explore the potential mechanism of the suppressive effects on tumors of RASSF1A and the relationship between RASSF1A and apoptosis or the proapoptosis protein MOAP-- 1 (modulator of apoptosis-1). Methods. HA-RASSF1A or Myc-- MOAP-- 1 was trans- fected into H1299 transiently or into HCT116 stably. Hela or the tranfsected cells were treated with TRIAL and detected the interaction between RASSF1A and MOAP--1 by CO--IP, Western Blot and confocal assays. Results: RASSFIA can interact with MOAP-1. RASSF1A co--localizes with MOAP--1 and up--regulates its protein level under TRAIL treatment. Conclusion.. RASSFIA is a regulator of MOAP--1 stability that can promote Bax--dependent apoptotic function in mitochondria through stabilization of MOAP-1 which may be the possible mechanism of tumor suppression.
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