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EMBO J. 2015 Apr 1;34(7):856-80. doi: 10.15252/embj.201490784. Epub 2015 Feb 23.

Autophagy in malignant transformation and cancer progression.

Author information

  • 1Equipe 11 labellisée pas la Ligue Nationale contre le Cancer, Centre de Recherche des Cordeliers, Paris, France INSERM U1138, Paris, France Gustave Roussy Cancer Campus, Villejuif, France Université Paris Descartes Sorbonne Paris Cité, Paris, France deadoc@vodafone.it.
  • 2Equipe 11 labellisée pas la Ligue Nationale contre le Cancer, Centre de Recherche des Cordeliers, Paris, France INSERM U1138, Paris, France Gustave Roussy Cancer Campus, Villejuif, France.
  • 3Abramson Cancer Center, University of Pennsylvania, Philadelphia, PA, USA.
  • 4Department of Molecular, Cell and Cancer Biology, University of Massachusetts Medical School, Worcester, MA, USA.
  • 5Cell Stress and Survival Unit, Danish Cancer Society Research Center, Copenhagen, Denmark IRCCS Fondazione Santa Lucia and Department of Biology University of Rome Tor Vergata, Rome, Italy.
  • 6Université Paris Descartes Sorbonne Paris Cité, Paris, France Institut Necker Enfants-Malades (INEM), Paris, France INSERM U1151, Paris, France CNRS UMR8253, Paris, France.
  • 7Department of Pathology and Helen Diller Family Comprehensive Cancer Center, University of California San Francisco, San Francisco, CA, USA.
  • 8Department of Pharmacology, Toxicology and Medicine, Virginia Commonwealth University, Richmond Virginia, VA, USA.
  • 9Merck Research Laboratories, Rahway, NJ, USA.
  • 10Division of Genomic Stability and DNA Repair, Department of Radiation Oncology, Dana-Farber Cancer Institute, Boston, MA, USA.
  • 11Centre for Cancer Biology, University of South Australia, Adelaide, SA, Australia.
  • 12Center for Autophagy Research, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX, USA Department of Microbiology, University of Texas Southwestern Medical Center, Dallas, TX, USA Howard Hughes Medical Institute, University of Texas Southwestern Medical Center, Dallas, TX, USA.
  • 13Department of Genetics, Trinity College, The Smurfit Institute, Dublin, Ireland.
  • 14Institute of Molecular Biotechnology of the Austrian Academy of Sciences, Vienna, Austria.
  • 15Department of Biology, University of Rome Tor Vergata, Rome, Italy National Institute for Infectious Diseases IRCCS 'Lazzaro Spallanzani', Rome, Italy.
  • 16Department of Medical Genetics, Cambridge Institute for Medical Research, University of Cambridge, Cambridge, UK.
  • 17Institute of Pharmacology, University of Bern, Bern, Switzerland.
  • 18Institute of Basic Medical Sciences, University of Oslo, Oslo, Norway.
  • 19Department of Pharmacology, University of Colorado School of Medicine, Aurora, CO, USA.
  • 20Department of Biochemistry and Molecular Biology I, School of Biology, Complutense University of Madrid, Madrid, Spain Instituto de Investigaciones Sanitarias San Carlos (IdISSC), Madrid, Spain.
  • 21Cancer Research UK Beatson Institute, Glasgow, UK.
  • 22Equipe 11 labellisée pas la Ligue Nationale contre le Cancer, Centre de Recherche des Cordeliers, Paris, France INSERM U1138, Paris, France Université Paris Descartes Sorbonne Paris Cité, Paris, France Pôle de Biologie, Hôpital Européen Georges Pompidou, AP-HP, Paris, France Metabolomics and Cell Biology Platforms, Gustave Roussy Cancer Campus, Villejuif, France.

Abstract

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.

© 2015 The Authors.

KEYWORDS:

Beclin 1; KRAS; adaptive stress responses; inflammation; mitophagy

PMID:
25712477
[PubMed - indexed for MEDLINE]
PMCID:
PMC4388596
Free PMC Article
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