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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Autophagy activity has been linked to development and progression of a plethora of pathologies.
“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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- 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 · 2014: 2
- 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
- Health Sciences › Medicine › Epidemiology › 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
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