钙蛋白酶介导的自噬相关蛋白5(Atg5)裂解会使自噬转变为凋亡。
Calpain-mediated cleavage of Atg5 switches autophagy to apoptosis.
作者信息
Yousefi Shida, Perozzo Remo, Schmid Inès, Ziemiecki Andrew, Schaffner Thomas, Scapozza Leonardo, Brunner Thomas, Simon Hans-Uwe
机构信息
Department of Pharmacology, University of Bern, CH-3010 Bern, Switzerland.
出版信息
Nat Cell Biol. 2006 Oct;8(10):1124-32. doi: 10.1038/ncb1482. Epub 2006 Sep 24.
Autophagy-related gene (Atg) 5 is a gene product required for the formation of autophagosomes. Here, we report that Atg5, in addition to the promotion of autophagy, enhances susceptibility towards apoptotic stimuli. Enforced expression of Atg5-sensitized tumour cells to anticancer drug treatment both in vitro and in vivo. In contrast, silencing the Atg5 gene with short interfering RNA (siRNA) resulted in partial resistance to chemotherapy. Apoptosis was associated with calpain-mediated Atg5 cleavage, resulting in an amino-terminal cleavage product with a relative molecular mass of 24,000 (Mr 24K). Atg5 cleavage was observed independent of the cell type and the apoptotic stimulus, suggesting that calpain activation and Atg5 cleavage are general phenomena in apoptotic cells. Truncated Atg5 translocated from the cytosol to mitochondria, associated with the anti-apoptotic molecule Bcl-xL and triggered cytochrome c release and caspase activation. Taken together, calpain-mediated Atg5 cleavage provokes apoptotic cell death, therefore, represents a molecular link between autophagy and apoptosis--a finding with potential importance for clinical anticancer therapies.
自噬相关基因(Atg)5是自噬体形成所需的一种基因产物。在此,我们报告Atg5除了促进自噬外,还增强了对凋亡刺激的敏感性。Atg5的强制表达使肿瘤细胞在体外和体内对抗癌药物治疗均敏感。相反,用小干扰RNA(siRNA)沉默Atg5基因导致对化疗产生部分抗性。凋亡与钙蛋白酶介导的Atg5裂解有关,产生相对分子质量为24000(Mr 24K)的氨基末端裂解产物。观察到Atg5裂解与细胞类型和凋亡刺激无关,这表明钙蛋白酶激活和Atg5裂解是凋亡细胞中的普遍现象。截短的Atg5从细胞质转移到线粒体,与抗凋亡分子Bcl-xL结合并触发细胞色素c释放和半胱天冬酶激活。综上所述,钙蛋白酶介导的Atg5裂解引发凋亡性细胞死亡,因此代表了自噬与凋亡之间的分子联系——这一发现对临床抗癌治疗具有潜在重要性。