Frezza Christian
Medical Research Council Cancer Unit, University of Cambridge, Hutchison/MRC Research Centre, Box 197, Cambridge Biomedical Campus, Cambridge CB2 0XZ, United Kingdom.
Int J Biochem Cell Biol. 2014 Mar;48:11-7. doi: 10.1016/j.biocel.2013.12.013. Epub 2014 Jan 4.
Mitochondria are intracellular organelles thought to have evolved from an alphaproteobacterium engulfed by the ancestor of the eukaryotic cell, an archeon, two billion years ago. Although mitochondria are frequently recognised as the "power plant" of the cell, the function of these organelles go beyond the simple generation of ATP. In fact, mounting evidence suggests that mitochondria are involved in several cellular processes, from regulation of cell death to signal transduction. Given this important role in cell physiology, mitochondrial dysfunction has been frequently associated with human diseases including cancer. Importantly, recent evidence suggests that mitochondrial function is directly regulated by oncogenes and tumour suppressors. However, the consequences of deregulation of mitochondrial function in tumour formation are still unclear. In this review, I propose that mitochondria play a pivotal role in shaping the oncogenic signalling cascade and that mitochondrial dysfunction, in some circumstances, is a required step for cancer transformation.
线粒体是细胞内的细胞器,被认为是由20亿年前被真核细胞(古细菌)的祖先吞噬的α-变形菌进化而来。尽管线粒体常被视为细胞的“动力工厂”,但其功能远不止于简单地产生ATP。事实上,越来越多的证据表明,线粒体参与了从细胞死亡调节到信号转导等多个细胞过程。鉴于其在细胞生理学中的这一重要作用,线粒体功能障碍常与包括癌症在内的人类疾病相关联。重要的是,最近的证据表明线粒体功能直接受癌基因和肿瘤抑制因子的调控。然而,线粒体功能失调在肿瘤形成中的后果仍不清楚。在这篇综述中,我提出线粒体在塑造致癌信号级联反应中起关键作用,并且在某些情况下,线粒体功能障碍是癌症转化的必要步骤。