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The autophagic network and cancer

Abstract

Mammalian cells harness autophagy to eliminate physiological byproducts of metabolism and cope with microenvironmental perturbations. Moreover, autophagy connects cellular adaptation with extracellular circuitries that impinge on immunity and metabolism. As it links transformed and non-transformed components of the tumour microenvironment, such an autophagic network is important for cancer initiation, progression and response to therapy. Here, we discuss the mechanisms whereby the autophagic network interfaces with multiple aspects of malignant disease.

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Fig. 1: General organization of autophagy and the autophagic network.
Fig. 2: Autophagic responses in pre-malignant and malignant cells.
Fig. 3: Impact of autophagic responses in endothelial and stromal cells of the neoplastic lesion on tumour progression and response to treatment.
Fig. 4: Impact of autophagic responses in immune cells on malignant transformation, tumour progression and response to treatment.

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Acknowledgements

G.K. is supported by the French Ligue contre le Cancer (équipe labellisée); Agence National de la Recherche (ANR) – Projets blancs; ANR under the frame of E-Rare-2, the ERA-Net for Research on Rare Diseases; Association pour la recherche sur le cancer (ARC); Cancéropôle Ile-de-France; Institut National du Cancer (INCa); Institut Universitaire de France; Fondation pour la Recherche Médicale (FRM); the European Commission (ArtForce); the European Research Council (ERC); the LeDucq Foundation; the LabEx Immuno-Oncology; the SIRIC Stratified Oncology Cell DNA Repair and Tumor Immune Elimination (SOCRATE); the SIRIC Cancer Research and Personalized Medicine (CARPEM); and the Paris Alliance of Cancer Research Institutes (PACRI). L.G. is supported by an intramural startup from the Department of Radiation Oncology of Weill Cornell Medical College (New York, USA) and by Sotio a.s. (Prague, Czech Republic).

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Rybstein, M.D., Bravo-San Pedro, J.M., Kroemer, G. et al. The autophagic network and cancer. Nat Cell Biol 20, 243–251 (2018). https://doi.org/10.1038/s41556-018-0042-2

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