| Literature DB >> 25712477 |
Lorenzo Galluzzi1, Federico Pietrocola2, José Manuel Bravo-San Pedro2, Ravi K Amaravadi3, Eric H Baehrecke4, Francesco Cecconi5, Patrice Codogno6, Jayanta Debnath7, David A Gewirtz8, Vassiliki Karantza9, Alec Kimmelman10, Sharad Kumar11, Beth Levine12, Maria Chiara Maiuri2, Seamus J Martin13, Josef Penninger14, Mauro Piacentini15, David C Rubinsztein16, Hans-Uwe Simon17, Anne Simonsen18, Andrew M Thorburn19, Guillermo Velasco20, Kevin M Ryan21, Guido Kroemer22.
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.Entities:
Keywords: Beclin 1; KRAS; adaptive stress responses; inflammation; mitophagy
Mesh:
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Year: 2015 PMID: 25712477 PMCID: PMC4388596 DOI: 10.15252/embj.201490784
Source DB: PubMed Journal: EMBO J ISSN: 0261-4189 Impact factor: 11.598