Mitochondria and cancer
Open accessAbstract
Mitochondria are bioenergetic, biosynthetic, and signaling organelles that are integral in stress sensing to allow for cellular adaptation to the environment. Therefore, it is not surprising that mitochondria are important mediators of tumorigenesis, as this process requires flexibility to adapt to cellular and environmental alterations in addition to cancer treatments. Multiple aspects of mitochondrial biology beyond bioenergetics support transformation, including mitochondrial biogenesis and turnover, fission and fusion dynamics, cell death susceptibility, oxidative stress regulation, metabolism, and signaling. Thus, understanding mechanisms of mitochondrial function during tumorigenesis will be critical for the next generation of cancer therapeutics.
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Mitochondrial-mediated flexibility is central in cancer metabolic flexibility.
“Mitochondrial-mediated flexibility is central in this process [reviewed in Vyas et al. (199)].”
From Metabolic Flexibility as an Adaptation to Energy Resources and Requirements in Health and Disease (2018) · cites this paper as [199]
Mitochondria coordinate cellular adaptation to stressors such as nutrient deprivation, oxidative stress, DNA damage and ER stress.
“Mitochondria coordinate cellular adaptation to stressors such as nutrient deprivation, oxidative stress, DNA damage and ER stress.5”
From The multifaceted contributions of mitochondria to cellular metabolism (2018) · cites this paper as [5]
Highly proliferative cells such as cancer cells and activated T cells rely on mitochondrial metabolites to form biomass.
“Rather than being dysfunctional, highly proliferative cells such as cancer cells and activated T cells rely on mitochondrial metabolites to form biomass.5,65”
From The multifaceted contributions of mitochondria to cellular metabolism (2018) · cites this paper as [5]
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The multifaceted contributions of mitochondria to cellular metabolism
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Metabolic recycling of ammonia via glutamate dehydrogenase supports breast cancer biomass
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“Mitochondria are highly dynamic reticular organelles whose number and morphology is continuously remodeled by fission and fusion [23].”
BackgroundFumarate is a terminal electron acceptor in the mammalian electron transport chain
Spinelli, J. B., Rosen, P. C., Sprenger, H.-G., Puszynska, A. M., Mann, J. L., Roessler, J. M., Cangelosi, A. L., Henne, A., Condon, K. J., Zhang, T., et al. (2021) · Science · doi:10.1126/science.abi7495 · Cited by 221 · see citing works
Telomerase and telomeres in aging theory and chronographic aging theory (Review)
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Zheng, F., Kelly, M. R., Ramms, D. J., Heintschel, M. L., Tao, K., Tutuncuoglu, B., Lee, J. J., Ono, K., Foussard, H., Chen, M., et al. (2021) · Science · doi:10.1126/science.abf3067 · Cited by 81 · see citing works
A novel lysosome‐to‐mitochondria signaling pathway disrupted by amyloid‐β oligomers
Norambuena, A., Wallrabe, H., Cao, R., Wang, D. B., Silva, A., Svindrych, Z., Periasamy, A., Hu, S., Tanzi, R. E., Kim, D. Y., et al. (2018) · The EMBO Journal · doi:10.15252/embj.2018100241 · Cited by 61 · see citing works
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Silva, E. A., Dalla Costa, A. P., Ruas, J. S., Siqueira-Santos, E. S., Francisco, A., & Castilho, R. F. (2023) · Cells · doi:10.3390/cells12050683 · Cited by 5 · see citing works
- Authors
- Vyas, S., Zaganjor, E., & Haigis, M. C.
- Affiliations
- Harvard University (US)
- Corresponding author
- Haigis, Marcia C.
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2016-07
- Volume
- 166
- Issue
- 3
- Pages
- 555-566
- ISSN
- 0092-8674 (ISSN-L)
- PMC
- PMC5036969
- OpenAlex
- W2480725775
- Cited by
- 1,735
- References
- 103
- Citations by year
- 2026: 145 · 2025: 173 · 2024: 199 · 2023: 190 · 2022: 184 · 2021: 230 · 2020: 215 · 2019: 176 · 2018: 112 · 2017: 94 · 2016: 16 · 2013: 1
- FWCI
- 12.01
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- American Cancer Society
- American Heart Association
- Ludwig Center at Harvard
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK103295)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Keywords
- mitochondria, cancer, carcinogenesis, mitochondrial biogenesis, mitochondrial fission and fusion, oxidative stress, cellular metabolism, cell death, mitochondrial signaling, cancer therapeutics, cellular adaptation
- MeSH terms
- Animals, Humans, Mitochondria, 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.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
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