Mathew Robin, Kongara Sameera, Beaudoin Brian, Karp Cristina M, Bray Kevin, Degenhardt Kurt, Chen Guanghua, Jin Shengkan, White Eileen
University of Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School, Piscataway, New Jersey 08854, USA.
Genes Dev. 2007 Jun 1;21(11):1367-81. doi: 10.1101/gad.1545107. Epub 2007 May 17.
Autophagy is a bulk degradation process that promotes survival under metabolic stress, but it can also be a means of cell death if executed to completion. Monoallelic loss of the essential autophagy gene beclin1 causes susceptibility to metabolic stress, but also promotes tumorigenesis. This raises the paradox that the loss of a survival pathway enhances tumor growth, where the exact mechanism is not known. Here, we show that compromised autophagy promoted chromosome instability. Failure to sustain metabolism through autophagy was associated with increased DNA damage, gene amplification, and aneuploidy, and this genomic instability may promote tumorigenesis. Thus, autophagy maintains metabolism and survival during metabolic stress that serves to protect the genome, providing an explanation for how the loss of a survival pathway leads to tumor progression. Identification of this novel role of autophagy may be important for rational chemotherapy and therapeutic exploitation of autophagy inducers as potential chemopreventive agents.
自噬是一种大量降解过程,在代谢应激下可促进细胞存活,但如果完全执行也可能成为细胞死亡的一种方式。必需自噬基因贝林1(beclin1)的单等位基因缺失会导致对代谢应激敏感,但也会促进肿瘤发生。这就产生了一个悖论,即一种生存途径的丧失却会增强肿瘤生长,而其确切机制尚不清楚。在此,我们表明自噬受损会促进染色体不稳定。无法通过自噬维持代谢与DNA损伤增加、基因扩增及非整倍体相关,而这种基因组不稳定可能促进肿瘤发生。因此,自噬在代谢应激期间维持代谢和细胞存活,从而保护基因组,这就解释了一种生存途径的丧失如何导致肿瘤进展。确定自噬的这一新作用对于合理化疗以及将自噬诱导剂作为潜在化学预防剂进行治疗性开发可能具有重要意义。