The role of mitochondria in the oncogenic signal transduction

被引:46
作者
Frezza, Christian [1 ]
机构
[1] Univ Cambridge, Hutchison MRC Res Ctr, MRC, Canc Unit, Cambridge CB2 0XZ, England
基金
英国医学研究理事会;
关键词
Cancer; Mitochondria; Signal transduction; Oncometabolite; Biochemistry; K-RAS; FUMARATE HYDRATASE; TYROSINE KINASE; CELL-SURVIVAL; CANCER; METABOLISM; PROTEIN; DYSFUNCTION; INHIBITION; COMPLEX;
D O I
10.1016/j.biocel.2013.12.013
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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. (c) 2014 Elsevier Ltd. All rights reserved.
引用
收藏
页码:11 / 17
页数:7
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