Akt Determines Replicative Senescence and Oxidative or Oncogenic Premature Senescence and Sensitizes Cells to Oxidative Apoptosis
Open accessAbstract
Akt deficiency causes resistance to replicative senescence, to oxidative stress- and oncogenic Ras-induced premature senescence, and to reactive oxygen species (ROS)-mediated apoptosis. Akt activation induces premature senescence and sensitizes cells to ROS-mediated apoptosis by increasing intracellular ROS through increased oxygen consumption and by inhibiting the expression of ROS scavengers downstream of FoxO, particularly sestrin 3. This uncovers an Achilles' heel of Akt, since in contrast to its ability to inhibit apoptosis induced by multiple apoptotic stimuli, Akt could not inhibit ROS-mediated apoptosis. Furthermore, treatment with rapamycin that led to further Akt activation and resistance to etoposide hypersensitized cancer cells to ROS-mediated apoptosis. Given that rapamycin alone is mainly cytostatic, this constitutes a strategy for cancer therapy that selectively eradicates cancer cells via Akt activation.
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Other DNA lesions, such as those from oxidative stress, may also drive senescence.
“Other DNA lesions—such as those caused by oxidative stress—may also drive cells into senescence (35–38).”
From Aging, Cellular Senescence, and Cancer (2013) · cites this paper as [37]
Akt activation is associated with increased oxygen consumption and an increase in total cellular ATP derived from both glycolytic and oxidative sources.
“Akt activation is associated with increased oxygen consumption as well as an increase in total cellular ATP derived from both glycolytic and oxidative sources 30, 31.”
From Mitochondrial reactive oxygen species regulate cellular signaling and dictate biological outcomes (2010) · cites this paper as [31]
Akt activation is associated with the accumulation of mitochondrial ROS.
“Akt activation is also associated with the accumulation of mitochondrial ROS 31.”
From Mitochondrial reactive oxygen species regulate cellular signaling and dictate biological outcomes (2010) · cites this paper as [31]
Compounds that raise ROS levels can effectively and selectively kill a variety of tumor cell lines.
“Indeed, this seems to be the case as compounds that raise ROS levels can effectively and selectively kill a variety of tumor cell lines 31, 74, 75.”
From Mitochondrial reactive oxygen species regulate cellular signaling and dictate biological outcomes (2010) · cites this paper as [31]
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- Authors
- Nogueira, V., Park, Y., Chen, C.-C., Xu, P.-Z., Chen, M.-L., Tonic, I., Unterman, T., & Hay, N.
- Affiliations
- University of Illinois Chicago (US)
- Corresponding author
- Hay, Nissim
- Venue
- Cancer Cell
- Publisher
- Elsevier BV
- Published
- 2008-12
- Volume
- 14
- Issue
- 6
- Pages
- 458-470
- ISSN
- 1535-6108 (ISSN-L)
- PMC
- PMC3038665
- OpenAlex
- W2132399579
- Cited by
- 780
- References
- 41
- Citations by year
- 2026: 14 · 2025: 18 · 2024: 33 · 2023: 45 · 2022: 57 · 2021: 68 · 2020: 35 · 2019: 37 · 2018: 54 · 2017: 44 · 2016: 41 · 2015: 52 · 2014: 44 · 2013: 61 · 2012: 48
- FWCI
- 28.65
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Cancer Cell (publishedVersion, other-oa)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- HAL (submittedVersion, cc-by)
- Funders
- National Institutes of Health
- University of Illinois at Chicago
- National Institute on Aging (AG 025953, R01AG025953, R01AG016927, AG016927)
- National Cancer Institute (CA090764, R01CA090764)
- Topics
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › FOXO transcription factor regulation
- Keywords
- Akt, replicative senescence, premature senescence, oxidative stress, oncogenic Ras, reactive oxygen species, FOXO, oxygen consumption, rapamycin, cancer therapy
- MeSH terms
- Forkhead Box Protein O1, Animals, Male, Neoplasms, Oxygen Consumption, RNA, Messenger, Signal Transduction, Gene Expression Regulation, Neoplastic, Cellular Senescence, Apoptosis, Reactive Oxygen Species, Mice, Knockout, Oxidative Stress, Sirolimus, Mice, Forkhead Transcription Factors
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Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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