【摘要】 Caspase非依赖性细胞程序性死亡(Caspase-independent cell death,CICD),是指在细胞程序性死亡中,Caspase不起主要作用,主要由PARP-1,Calpains,Bax及AIF 4种蛋白依次激活而启动,并具有不同于凋亡和坏死的生物学特点。近年来研究认为,通过CICD途径诱导K562细胞死亡不同于以往药物杀死白血病细胞的作用机制,有望成为一种新的药物作用靶点。本文综述了近年来对于CICD分子机制的最新认识,以及诱导K562细胞发生CICD的相关研究,以期为研究耐药肿瘤细胞药物作用新靶点提供参考。更多还原

【Abstract】 Caspase independent cell death(CICD)is defined as death that ensues when a signal that normally induces apoptosis fails to activate caspasesit can be activated by PARP-1CalpainsBax and AIFpossessing distinctive biologic characteristic differed from apoptosis and necrosis.Recent researchs have found that the molecular mechanisms governing CICD of K562 is opposite from that of the traditional medicine killing leukemia cellswhich may have the potential pharmaceutical point for new drugs.This article reviews the newly acquaintance of molecular mechanisms for CICD and recent studies concerning the induction death of K562 cells via CICDso as to provide some reference for the research of new drug point.更多还原