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Autophagy and Tumor Metabolism
Open accessAbstract
Autophagy is a critical cellular process that generally protects cells and organisms from stressors such as nutrient deprivation. In addition to its role in normal physiology, autophagy plays a role in pathological processes such as cancer. Indeed, there has been substantial work exploring the complex and context-dependent role of autophagy in cancer. One of the emerging themes is that in certain cancer types, autophagy is important to support tumor growth; therefore, inhibiting autophagy as a therapeutic approach is actively being tested in clinical trials. A key mechanism of how autophagy promotes the growth and survival of various cancers is its ability to support cellular metabolism. The diverse metabolic fuel sources that can be produced by autophagy provide tumors with metabolic plasticity and can allow them to thrive in what can be an austere microenvironment. Therefore, understanding how autophagy can fuel cellular metabolism will enable more effective combinatorial therapeutic strategies.
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“Autophagy is upregulated in KRAS mutant cancer cells and it serves as a cell survival mechanism when cancer cells experience metabolic stress (97).”
From KRAS mutation in pancreatic cancer (2021) · cites this paper as [97]
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“Autophagy is upregulated in KRAS mutant cancer cells and it serves as a cell survival mechanism when cancer cells experience metabolic stress (97).”
From KRAS mutation in pancreatic cancer (2021) · cites this paper as [97]
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“According to a recurrent scenario, once a potentially tumorigenic clone has emerged, autophagy must be (re)activated to improve cellular fitness and to facilitate the transition to full-blown malignancy.164”
From Meta-hallmarks of aging and cancer (2023) · cites this paper as [164]
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Metadata
- Authors
- Kimmelman, A. C., & White, E.
- Affiliations
- NYU Langone Health (US)
- Rutgers, The State University of New Jersey (US)
- Corresponding author
- Kimmelman, Alec C.
- White, Eileen
- Venue
- Cell Metabolism
- Publisher
- Elsevier BV
- Published
- 2017-05
- Volume
- 25
- Issue
- 5
- Pages
- 1037-1043
- ISSN
- 1550-4131 (ISSN-L)
- PMC
- PMC5604466
- OpenAlex
- W2611224317
- Cited by
- 826
- References
- 80
- Citations by year
- 2026: 37 · 2025: 58 · 2024: 99 · 2023: 88 · 2022: 109 · 2021: 150 · 2020: 112 · 2019: 95 · 2018: 61 · 2017: 17
- FWCI
- 10.33
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell Metabolism (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Cancer Institute (R01CA157490, R01CA188048, P01CA117969)
- ACS (RSG-13-298-01-TBG)
- NIH (R01GM095567, R01CA163591, R01CA130893, R01CA188096, R01CA193970)
- Robert Wood Johnson Foundation (P30CA72720)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Autophagy in Disease and Therapy
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Keywords
- autophagy, cancer metabolism, cancer, metabolic plasticity, nutrient deprivation, autophagy inhibition, cancer therapy, tumor microenvironment, tumor growth
- MeSH terms
- Animals, Autophagy, Cell Survival, Humans, Neoplasms, Cell Proliferation, Metabolic Networks and Pathways, Tumor Microenvironment
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