Recent insights into the function of autophagy in cancer
Macroautophagy (referred to here as autophagy) is induced by starvation to capture and degrade intracellular proteins and organelles in lysosomes, which recycles intracellular components to sustain metabolism and survival. Autophagy also plays a major homeostatic role in controlling protein and orga...
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| Published in | Genes & development Vol. 30; no. 17; pp. 1913 - 1930 |
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| Main Authors | , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Cold Spring Harbor Laboratory Press
01.09.2016
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| Subjects | |
| Online Access | Get full text |
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| Abstract | Macroautophagy (referred to here as autophagy) is induced by starvation to capture and degrade intracellular proteins and organelles in lysosomes, which recycles intracellular components to sustain metabolism and survival. Autophagy also plays a major homeostatic role in controlling protein and organelle quality and quantity. Dysfunctional autophagy contributes to many diseases. In cancer, autophagy can be neutral, tumor-suppressive, or tumor-promoting in different contexts. Large-scale genomic analysis of human cancers indicates that the loss or mutation of core autophagy genes is uncommon, whereas oncogenic events that activate autophagy and lysosomal biogenesis have been identified. Autophagic flux, however, is difficult to measure in human tumor samples, making functional assessment of autophagy problematic in a clinical setting. Autophagy impacts cellular metabolism, the proteome, and organelle numbers and quality, which alter cell functions in diverse ways. Moreover, autophagy influences the interaction between the tumor and the host by promoting stress adaptation and suppressing activation of innate and adaptive immune responses. Additionally, autophagy can promote a cross-talk between the tumor and the stroma, which can support tumor growth, particularly in a nutrient-limited microenvironment. Thus, the role of autophagy in cancer is determined by nutrient availability, microenvironment stress, and the presence of an immune system. Here we discuss recent developments in the role of autophagy in cancer, in particular how autophagy can promote cancer through suppressing p53 and preventing energy crisis, cell death, senescence, and an anti-tumor immune response. |
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| AbstractList | In this review, Amaravadi et al. discuss recent developments in the role of autophagy in cancer, in particular how autophagy can promote cancer through suppressing p53 and preventing energy crisis, cell death, senescence, and an anti-tumor immune response.
Macroautophagy (referred to here as autophagy) is induced by starvation to capture and degrade intracellular proteins and organelles in lysosomes, which recycles intracellular components to sustain metabolism and survival. Autophagy also plays a major homeostatic role in controlling protein and organelle quality and quantity. Dysfunctional autophagy contributes to many diseases. In cancer, autophagy can be neutral, tumor-suppressive, or tumor-promoting in different contexts. Large-scale genomic analysis of human cancers indicates that the loss or mutation of core autophagy genes is uncommon, whereas oncogenic events that activate autophagy and lysosomal biogenesis have been identified. Autophagic flux, however, is difficult to measure in human tumor samples, making functional assessment of autophagy problematic in a clinical setting. Autophagy impacts cellular metabolism, the proteome, and organelle numbers and quality, which alter cell functions in diverse ways. Moreover, autophagy influences the interaction between the tumor and the host by promoting stress adaptation and suppressing activation of innate and adaptive immune responses. Additionally, autophagy can promote a cross-talk between the tumor and the stroma, which can support tumor growth, particularly in a nutrient-limited microenvironment. Thus, the role of autophagy in cancer is determined by nutrient availability, microenvironment stress, and the presence of an immune system. Here we discuss recent developments in the role of autophagy in cancer, in particular how autophagy can promote cancer through suppressing p53 and preventing energy crisis, cell death, senescence, and an anti-tumor immune response. Macroautophagy (referred to here as autophagy) is induced by starvation to capture and degrade intracellular proteins and organelles in lysosomes, which recycles intracellular components to sustain metabolism and survival. Autophagy also plays a major homeostatic role in controlling protein and organelle quality and quantity. Dysfunctional autophagy contributes to many diseases. In cancer, autophagy can be neutral, tumor-suppressive, or tumor-promoting in different contexts. Large-scale genomic analysis of human cancers indicates that the loss or mutation of core autophagy genes is uncommon, whereas oncogenic events that activate autophagy and lysosomal biogenesis have been identified. Autophagic flux, however, is difficult to measure in human tumor samples, making functional assessment of autophagy problematic in a clinical setting. Autophagy impacts cellular metabolism, the proteome, and organelle numbers and quality, which alter cell functions in diverse ways. Moreover, autophagy influences the interaction between the tumor and the host by promoting stress adaptation and suppressing activation of innate and adaptive immune responses. Additionally, autophagy can promote a cross-talk between the tumor and the stroma, which can support tumor growth, particularly in a nutrient-limited microenvironment. Thus, the role of autophagy in cancer is determined by nutrient availability, microenvironment stress, and the presence of an immune system. Here we discuss recent developments in the role of autophagy in cancer, in particular how autophagy can promote cancer through suppressing p53 and preventing energy crisis, cell death, senescence, and an anti-tumor immune response. |
| Author | White, Eileen Amaravadi, Ravi Kimmelman, Alec C. |
| AuthorAffiliation | 5 Rutgers Cancer Institute of New Jersey, New Brunswick, New Jersey 08903, USA 2 Department of Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA 6 Department of Molecular Biology and Biochemistry, Rutgers University, Piscataway, New Jersey 08854, USA 3 Perlmutter Cancer Center, New York University Langone Medical Center, New York, New York 10016, USA 4 Department of Radiation Oncology, New York University Langone Medical Center, New York, New York 10016, USA 1 Abramson Cancer Center, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA |
| AuthorAffiliation_xml | – name: 1 Abramson Cancer Center, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA – name: 5 Rutgers Cancer Institute of New Jersey, New Brunswick, New Jersey 08903, USA – name: 4 Department of Radiation Oncology, New York University Langone Medical Center, New York, New York 10016, USA – name: 6 Department of Molecular Biology and Biochemistry, Rutgers University, Piscataway, New Jersey 08854, USA – name: 2 Department of Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA – name: 3 Perlmutter Cancer Center, New York University Langone Medical Center, New York, New York 10016, USA |
| Author_xml | – sequence: 1 givenname: Ravi surname: Amaravadi fullname: Amaravadi, Ravi – sequence: 2 givenname: Alec C. surname: Kimmelman fullname: Kimmelman, Alec C. – sequence: 3 givenname: Eileen surname: White fullname: White, Eileen |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/27664235$$D View this record in MEDLINE/PubMed |
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| Copyright | 2016 Amaravadi et al.; Published by Cold Spring Harbor Laboratory Press. 2016 |
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| Issue | 17 |
| Keywords | chloroquine mouse models cancer autophagy ATG |
| Language | English |
| License | 2016 Amaravadi et al.; Published by Cold Spring Harbor Laboratory Press. This article is distributed exclusively by Cold Spring Harbor Laboratory Press for the first six months after the full-issue publication date (see http://genesdev.cshlp.org/site/misc/terms.xhtml). After six months, it is available under a Creative Commons License (Attribution-NonCommercial 4.0 International), as described at http://creativecommons.org/licenses/by-nc/4.0/. |
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| Snippet | Macroautophagy (referred to here as autophagy) is induced by starvation to capture and degrade intracellular proteins and organelles in lysosomes, which... In this review, Amaravadi et al. discuss recent developments in the role of autophagy in cancer, in particular how autophagy can promote cancer through... |
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| SubjectTerms | Animals Autophagy - genetics Autophagy - physiology Disease Models, Animal Drug Delivery Systems Gene Expression Regulation, Neoplastic Humans Neoplasms - genetics Neoplasms - physiopathology Review |
| Title | Recent insights into the function of autophagy in cancer |
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