Journal article

Autophagy in malignant transformation and cancer progression.

  • Galluzzi L Equipe 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.
  • Pietrocola F Equipe 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.
  • Bravo-San Pedro JM Equipe 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.
  • Amaravadi RK Abramson Cancer Center, University of Pennsylvania, Philadelphia, PA, USA.
  • Baehrecke EH Department of Molecular, Cell and Cancer Biology, University of Massachusetts Medical School, Worcester, MA, USA.
  • Cecconi F Cell 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.
  • Codogno P Université Paris Descartes Sorbonne Paris Cité, Paris, France Institut Necker Enfants-Malades (INEM), Paris, France INSERM U1151, Paris, France CNRS UMR8253, Paris, France.
  • Debnath J Department of Pathology and Helen Diller Family Comprehensive Cancer Center, University of California San Francisco, San Francisco, CA, USA.
  • Gewirtz DA Department of Pharmacology, Toxicology and Medicine, Virginia Commonwealth University, Richmond Virginia, VA, USA.
  • Karantza V Merck Research Laboratories, Rahway, NJ, USA.
  • Kimmelman A Division of Genomic Stability and DNA Repair, Department of Radiation Oncology, Dana-Farber Cancer Institute, Boston, MA, USA.
  • Kumar S Centre for Cancer Biology, University of South Australia, Adelaide, SA, Australia.
  • Levine B Center 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.
  • Maiuri MC Equipe 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.
  • Martin SJ Department of Genetics, Trinity College, The Smurfit Institute, Dublin, Ireland.
  • Penninger J Institute of Molecular Biotechnology of the Austrian Academy of Sciences, Vienna, Austria.
  • Piacentini M Department of Biology, University of Rome Tor Vergata, Rome, Italy National Institute for Infectious Diseases IRCCS 'Lazzaro Spallanzani', Rome, Italy.
  • Rubinsztein DC Department of Medical Genetics, Cambridge Institute for Medical Research, University of Cambridge, Cambridge, UK.
  • Simon HU Institute of Pharmacology, University of Bern, Bern, Switzerland.
  • Simonsen A Institute of Basic Medical Sciences, University of Oslo, Oslo, Norway.
  • Thorburn AM Department of Pharmacology, University of Colorado School of Medicine, Aurora, CO, USA.
  • Velasco G Department of Biochemistry and Molecular Biology I, School of Biology, Complutense University of Madrid, Madrid, Spain Instituto de Investigaciones Sanitarias San Carlos (IdISSC), Madrid, Spain.
  • Ryan KM Cancer Research UK Beatson Institute, Glasgow, UK.
  • Kroemer G Equipe 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.
Show more…
  • 2015-02-26
Published in:
  • The EMBO journal. - 2015
English 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.
Language
  • English
Open access status
green
Identifiers
Persistent URL
https://folia.unifr.ch/global/documents/89681
Statistics

Document views: 8 File downloads:
  • fulltext.pdf: 0