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The role for autophagy in cancer
Open accessAbstract
Autophagy is a survival-promoting pathway that captures, degrades, and recycles intracellular proteins and organelles in lysosomes. Autophagy preserves organelle function, prevents the toxic buildup of cellular waste products, and provides substrates to sustain metabolism in starvation. Although in some contexts autophagy suppresses tumorigenesis, in most contexts autophagy facilitates tumorigenesis. Cancers can upregulate autophagy to survive microenvironmental stress and to increase growth and aggressiveness. Mechanisms by which autophagy promotes cancer include suppressing induction of the p53 tumor suppressor protein and maintaining metabolic function of mitochondria. Efforts to inhibit autophagy to improve cancer therapy have thereby attracted great interest.
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“Of note, since autophagy activity has been linked to development and progression of a plethora of pathologies [9–11], it becomes increasingly fundamental to develop new strategies for the prediction of a specific autophagy status and/or step [8].”
From A gene toolbox for monitoring autophagy transcription (2021) · cites this paper as [11]
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Metadata
- Authors
- White, E.
- Corresponding author
- White, Eileen
- ORCID
- White, Eileen
- Venue
- Journal of Clinical Investigation
- Published
- 2015-01-02
- Volume
- 125
- Issue
- 1
- Pages
- 42-46
- ISSN
- 0021-9738 (ISSN-L)
- PMC
- PMC4382247
- OpenAlex
- W2055811314
- Cited by
- 1,332
- References
- 58
- Citations by year
- 2026: 63 · 2025: 68 · 2024: 111 · 2023: 116 · 2022: 129 · 2021: 158 · 2020: 157 · 2019: 138 · 2018: 142 · 2017: 132 · 2016: 92 · 2015: 24
- FWCI
- 16.89
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Clinical Investigation (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Rutgers Cancer Institute of New Jersey
- National Institutes of Health
- National Cancer Institute (R01CA053370, R37CA053370, RC1CA147961, R01CA130893, R01CA163591)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Autophagy in Disease and Therapy
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ubiquitin and proteasome pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Physiology › Calcium signaling and nucleotide metabolism
- Keywords
- autophagy, cancer, carcinogenesis, lysosomes, p53, mitochondrial metabolism, tumor microenvironment, starvation, cancer therapy, autophagy inhibition
- MeSH terms
- Animals, Autophagy, Humans, Neoplasms, Carcinogenesis
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
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