Autophagy in malignant transformation and cancer progression

被引：1378

作者：

Galluzzi, Lorenzo ^{[1
,2
,3
,4
]}

Pietrocola, Federico ^{[1
,2
,3
]}

Bravo-San Pedro, Jose Manuel ^{[1
,2
,3
]}

Amaravadi, Ravi K. ^{[5
]}

Baehrecke, Eric H. ^{[6
]}

Cecconi, Francesco ^{[7
,8
,9
]}

Codogno, Patrice ^{[4
,10
,11
,12
]}

Debnath, Jayanta ^{[13
,14
]}

Gewirtz, David A. ^{[15
]}

Karantza, Vassiliki ^{[16
]}

Kimmelman, Alec ^{[17
]}

Kumar, Sharad ^{[18
]}

Levine, Beth ^{[19
,20
,21
]}

Maiuri, Maria Chiara ^{[1
,2
,3
]}

Martin, Seamus J. ^{[22
]}

Penninger, Josef ^{[23
]}

Piacentini, Mauro ^{[9
,24
]}

Rubinsztein, David C. ^{[25
]}

Simon, Hans-Uwe ^{[26
]}

Simonsen, Anne ^{[27
]}

Thorburn, Andrew M. ^{[28
]}

Velasco, Guillermo ^{[29
,30
]}

Ryan, Kevin M. ^{[31
]}

Kroemer, Guido ^{[1
,2
,4
,32
,33
]}

机构：

[1] Ctr Rech Cordeliers, Equipe Labellisee Pas Ligue Natl Canc 11, Paris, France

[2] INSERM, U1138, Paris, France

[3] Gustave Roussy Canc Campus, Villejuif, France

[4] Univ Paris 05, Sorbonne Paris Cite, Paris, France

[5] Univ Penn, Abramson Canc Ctr, Philadelphia, PA 19104 USA

[6] Univ Massachusetts, Sch Med, Dept Mol Cell & Canc Biol, Worcester, MA USA

[7] Danish Canc Soc Res Ctr, Cell Stress & Survival Unit, Copenhagen, Denmark

[8] Univ Roma Tor Vergata, IRCCS Fdn Santa Lucia, Rome, Italy

[9] Univ Roma Tor Vergata, Dept Biol, I-00173 Rome, Italy

[10] INEM, Paris, France

[11] INSERM, U1151, Paris, France

[12] CNRS, UMR8253, Paris, France

[13] Univ Calif San Francisco, Dept Pathol, San Francisco, CA 94140 USA

[14] Univ Calif San Francisco, Helen Diller Family Comprehens Canc Ctr, San Francisco, CA 94143 USA

[15] Virginia Commonwealth Univ, Dept Pharmacol Toxicol & Med, Richmond, VA USA

[16] Merck Res Labs, Rahway, NJ USA

[17] Dana Farber Canc Inst, Dept Radiat Oncol, Div Genom Stabil & DNA Repair, Boston, MA 02115 USA

[18] Univ S Australia, Ctr Canc Biol, Adelaide, SA 5001, Australia

[19] Univ Texas SW Med Ctr Dallas, Dept Internal Med, Ctr Autophagy Res, Dallas, TX 75390 USA

[20] Univ Texas SW Med Ctr Dallas, Dept Microbiol, Dallas, TX 75390 USA

[21] Univ Texas SW Med Ctr Dallas, Howard Hughes Med Inst, Dallas, TX 75390 USA

[22] Trinity Coll Dublin, Smurfit Inst, Dept Genet, Dublin, Ireland

[23] Austrian Acad Sci, Inst Mol Biotechnol, A-1010 Vienna, Austria

[24] Natl Inst Infect Dis IRCCS Lazzaro Spallanzani, Rome, Italy

[25] Univ Cambridge, Cambridge Inst Med Res, Dept Med Genet, Cambridge, England

[26] Univ Bern, Inst Pharmacol, Bern, Switzerland

[27] Univ Oslo, Inst Basic Med Sci, Oslo, Norway

[28] Univ Colorado, Sch Med, Dept Pharmacol, Aurora, CO USA

[29] Univ Complutense Madrid, Sch Biol, Dept Biochem & Mol Biol 1, Madrid, Spain

[30] IdISSC, Madrid, Spain

[31] Canc Res UK Beatson Inst, Glasgow, Lanark, Scotland

[32] Hop Europeen Georges Pompidou, AP HP, Pole Biol, Paris, France

[33] Gustave Roussy Canc Campus, Metabol & Cell Biol Platforms, Villejuif, France

来源：

EMBO JOURNAL | 2015年 / 34卷 / 07期

基金：

瑞士国家科学基金会; 欧洲研究理事会; 英国医学研究理事会;

关键词：

adaptive stress responses; Beclin; 1; inflammation; KRAS; mitophagy; TUMOR-SUPPRESSOR GENE; STRESS-INDUCED AUTOPHAGY; ADVANCED SOLID TUMORS; PHASE-I TRIAL; BCL-X-L; CELL-DEATH; BREAST-CANCER; BECLIN; DOWN-REGULATION; REGULATES AUTOPHAGY;

D O I：

10.15252/embj.201490784

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

070307 [化学生物学]; 071010 [生物化学与分子生物学];

摘要：

Autophagy plays a key role in the maintenance of cellular homeostasis. In healthy cells, such a homeostatic activity constitutes a robust barrier against malignant transformation. Accordingly, many oncoproteins inhibit, and several oncosuppressor proteins promote, autophagy. Moreover, autophagy is required for optimal anticancer immunosurveillance. In neoplastic cells, however, autophagic responses constitute a means to cope with intracellular and environmental stress, thus favoring tumor progression. This implies that at least in some cases, oncogenesis proceeds along with a temporary inhibition of autophagy or a gain of molecular functions that antagonize its oncosuppressive activity. Here, we discuss the differential impact of autophagy on distinct phases of tumorigenesis and the implications of this concept for the use of autophagy modulators in cancer therapy.

引用

页码：856 / 880

页数：25

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