Autophagy in tumour suppression and promotion

被引:357
作者
Brech, Andreas [1 ,2 ]
Ahlquist, Terje [2 ,3 ]
Lothe, Ragnhild A. [2 ,3 ]
Stenmark, Harald [1 ,2 ]
机构
[1] Oslo Univ Hosp, Norwegian Radium Hosp, Inst Canc Res, Dept Biochem, N-0310 Oslo, Norway
[2] Univ Oslo, Fac Med, Ctr Canc Biomed, N-0310 Oslo, Norway
[3] Oslo Univ Hosp, Norwegian Radium Hosp, Inst Canc Res, Dept Canc Prevent, N-0310 Oslo, Norway
关键词
Apoptosis; Autophagy; Beclin; 1; Carcinogenesis; Genome instability; Lysosome; PI; 3-kinase; Survival; Reactive oxygen species; UVRAG; CELL-DEATH; CANCER-CELLS; PROTEIN-DEGRADATION; INDUCED APOPTOSIS; CARCINOMA-CELLS; AMINO-ACIDS; INHIBITION; MTOR; PATHWAY; COMPLEX;
D O I
10.1016/j.molonc.2009.05.007
中图分类号
R73 [肿瘤学];
学科分类号
100214 [肿瘤学];
摘要
Autophagy, a well-described cellular mechanism for lysosomal degradation of cytoplasmic content, has emerged as a tumour suppression pathway. Recent evidence indicates that the tumour suppressor function of autophagy is mediated by scavenging of damaged oxidative organelles, thereby preventing accumulation of toxic oxygen radicals that would cause genome instability. Paradoxically, however, in some cases autophagy can also promote the survival of cancer cells once tumours have developed. This is attributed to the ability of autophagy to promote cell survival under conditions of poor nutrient supply, as often faced by solid tumours and metastasising cancer cells. In addition, autophagy is frequently upregulated in tumours as a response to therapy and may protect tumours against therapy-induced apoptosis. in this review we discuss the mechanisms that link autophagy to tumour suppression and promotion and provide examples of the dual functions of autophagy in cancer. (C) 2009 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
引用
收藏
页码:366 / 375
页数:10
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