期刊
EMBO JOURNAL
卷 34, 期 7, 页码 856-880出版社
WILEY
DOI: 10.15252/embj.201490784
关键词
adaptive stress responses; Beclin 1; inflammation; KRAS; mitophagy
资金
- Ligue contre le Cancer (equipe labelisee)
- Agence National de la Recherche (ANR)
- Association pour la recherche sur le cancer (ARC)
- Canceropole Ile-de-France
- Institut National du Cancer (INCa)
- Fondation Bettencourt-Schueller
- Fondation de France
- Fondation pour la Recherche Medicale (FRM)
- European Commission (ArtForce)
- European Research Council (ERC)
- LabEx Immuno-Oncology
- SIRIC Stratified Oncology Cell DNA Repair and Tumor Immune Elimination (SOCRATE)
- SIRIC Cancer Research and Personalized Medicine (CARPEM)
- Paris Alliance of Cancer Research Institutes (PACRI)
- American Cancer Society [IRG-14-192-40]
- National Health and Medical Research Council of Australia [1041807, 1002863]
- Ministry of Health of Italy ('Ricerca Corrente')
- Ministry of Health of Italy ('Ricerca Finalizzata')
- Associazione Italiana per la Ricerca sul Cancro (AIRC)
- Swiss National Science Foundation
- Swiss Cancer League
- European Commission (MEL-PLEX)
- Spanish Ministry of Economy and Competitiveness (MINECO)
- Fondo Europeo de Desarrollo Regional (FEDER) [PI12/02248, FR2009-0052, IT2009-0053]
- Fundacion Mutua Madrilena [AP101042012]
- Fundacio La Marato de TV3 [20134031]
- Cancer Research UK [15816] Funding Source: researchfish
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.
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