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
相关论文
共 105 条
  • [71] Myotonic dystrophy protein kinase (DMPK) prevents ROS-induced cell death by assembling a hexokinase II-Src complex on the mitochondrial surface
    Pantic, B.
    Trevisan, E.
    Citta, A.
    Rigobello, M. P.
    Marin, O.
    Bernardi, P.
    Salvatori, S.
    Rasola, A.
    [J]. CELL DEATH & DISEASE, 2013, 4 : e858 - e858
  • [72] Electrostatic interactions positively regulate K-ras nanocluster formation and function
    Plowman, Sarah J.
    Ariotti, Nicholas
    Goodall, Andrew
    Parton, Robert G.
    Hancock, John F.
    [J]. MOLECULAR AND CELLULAR BIOLOGY, 2008, 28 (13) : 4377 - 4385
  • [73] miR-210 is overexpressed in late stages of lung cancer and mediates mitochondrial alterations associated with modulation of HIF-1 activity
    Puissegur, M-P
    Mazure, N. M.
    Bertero, T.
    Pradelli, L.
    Grosso, S.
    Robbe-Sermesant, K.
    Maurin, T.
    Lebrigand, K.
    Cardinaud, B.
    Hofman, V.
    Fourre, S.
    Magnone, V.
    Ricci, J. E.
    Pouyssegur, J.
    Gounon, P.
    Hofman, P.
    Barbry, P.
    Mari, B.
    [J]. CELL DEATH AND DIFFERENTIATION, 2011, 18 (03) : 465 - 478
  • [74] RAS oncogenes: weaving a tumorigenic web
    Pylayeva-Gupta, Yuliya
    Grabocka, Elda
    Bar-Sagi, Dafna
    [J]. NATURE REVIEWS CANCER, 2011, 11 (11) : 761 - 774
  • [75] Activation of mitochondrial ERK protects cancer cells from death through inhibition of the permeability transition
    Rasola, Andrea
    Sciacovelli, Marco
    Chiara, Federica
    Pantic, Boris
    Brusilow, William S.
    Bernardi, Paolo
    [J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2010, 107 (02) : 726 - 731
  • [76] Catalytic competence of the Ras-GEF domain of hSos1 requires intra-REM domain interactions mediated by phenylalanine 577
    Sacco, Elena
    Metalli, David
    Busti, Stefano
    Fantinato, Sonia
    D'Urzo, Annalisa
    Mapelli, Valeria
    Alberghina, Lilia
    Vanoni, Marco
    [J]. FEBS LETTERS, 2006, 580 (27) : 6322 - 6328
  • [77] Mitochondrial disease
    Schapira, Anthony H. V.
    [J]. LANCET, 2006, 368 (9529) : 70 - 82
  • [78] SCHUMACHER HR, 1973, AM J PATHOL, V73, P27
  • [79] SCHUMACHER HR, 1973, LANCET, V2, P327
  • [80] SCHUMACHER HR, 1973, LANCET, V2, P1207