期刊
SEMINARS IN CANCER BIOLOGY
卷 23, 期 5, 页码 310-322出版社
ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.semcancer.2013.05.008
关键词
AMPK; Beclin 1; Cancer; Mitophagy; mTOR; PKR
类别
资金
- European Commission (ArtForce)
- Agence National de la Recherche (ANR)
- Ligue Nationale contre le Cancer
- Fondation pour la Recherche Medicale (FRM)
- Institut National du Cancer (INCa)
- Association pour la Recherche sur le Cancer (ARC)
- LabEx Immuno-Oncologie
- Fondation de France
- Fondation Bettencourt-Schueller
- AXA Chair for Longevity Research
- Canceropole Ile-de-France
- Paris Alliance of Cancer Research Institutes (PACRI)
- Cancer Research for Personalized Medicine (CARPEM)
Autophagy is an evolutionarily conserved process that promotes the lysosomal degradation of intracellular components including organelles and portions of the cytoplasm. Besides operating as a quality control mechanism in steady-state conditions, autophagy is upregulated in response to a variety of homeostatic perturbations. In this setting, autophagy mediates prominent cytoprotective effects as it sustains energetic homeostasis and contributes to the removal of cytotoxic stimuli, thus orchestrating a cell-wide, multipronged adaptive response to stress. In line with the critical role of autophagy in health and disease, defects in the autophagic machinery as well as in autophagy-regulatory signaling pathways have been associated with multiple human pathologies, including neurodegenerative disorders, autoimmune conditions and cancer. Accumulating evidence indicates that the autophagic response to stress may proceed in two phases. Thus, a rapid increase in the autophagic flux, which occurs within minutes or hours of exposure to stressful conditions and is entirely mediated by post-translational protein modifications, is generally followed by a delayed and protracted autophagic response that relies on the activation of specific transcriptional programs. Stress-responsive transcription factors including p53, NF-kappa B and STAT3 have recently been shown to play a major role in the regulation of both these phases of the autophagic response. Here, we will discuss the molecular mechanisms whereby autophagy is orchestrated by stress-responsive transcription factors. (C) 2013 Elsevier Ltd. All rights reserved.
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