Genetic deletion of Nrf2 promotes immortalization and decreases life span of murine embryonic fibroblasts
Open accessAbstract
Nuclear factor E2-related factor-2 (Nrf2) transcription factor is one of the main regulators of intracellular redox balance and a sensor of oxidative and electrophilic stress. Low Nrf2 activity is usually associated with carcinogenesis, but Nrf2 is also considered as an oncogene because it increases survival of transformed cells. Because intracellular redox balance alterations are involved in both senescence and tumorigenesis, we investigated the impact of Nrf2 genetic deletion on cellular immortalization and life span of murine embryonic fibroblasts. We report that Nrf2 genetic deletion promotes immortalization due to an early loss of p53-dependent gene expression. However, compared with control cells, immortalized Nrf2-/- murine embryonic fibroblasts exhibited decreased growth, lower cyclin E levels, and impaired expression of NQO1 and cytochrome b₅ reductase. Moreover, SirT1 was also significantly reduced in immortalized Nrf2-/- murine embryonic fibroblasts, and these cells exhibited shorter life span. Our results underscore the dual role of Nrf2 in protection against carcinogenesis and in the delay of cellular aging.
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Nrf2−/− MEFs are prone to immortalization but also show a short lifespan.
“Nrf2−/− MEFs were prone to immortalization but also showed a short lifespan”
From Rapamycin inhibits the secretory phenotype of senescent cells by a Nrf2-independent mechanism (2017) · cites this paper as Jodar et al., 2011
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- Authors
- Jodar, L., Mercken, E. M., Ariza, J., Younts, C., Gonzalez-Reyes, J. A., Alcain, F. J., Buron, I., de Cabo, R., & Villalba, J. M.
- Affiliations
- National Institutes of Health (US)
- University of Córdoba (ES)
- Venue
- The Journals of Gerontology Series A: Biological Sciences and Medical Sciences
- Publisher
- Oxford University Press (OUP)
- Published
- 2010-10-25
- Volume
- 66A
- Issue
- 3
- Pages
- 247-256
- ISSN
- 1079-5006 (ISSN-L)
- 1758-535X
- PMC
- PMC4007826
- OpenAlex
- W2131611717
- Cited by
- 33
- References
- 54
- Citations by year
- 2026: 1 · 2024: 1 · 2023: 1 · 2022: 4 · 2021: 1 · 2020: 3 · 2019: 1 · 2018: 6 · 2017: 2 · 2016: 3 · 2015: 2 · 2014: 1 · 2012: 6
- FWCI
- 0.91
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- The Journals of Gerontology Series A (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Universidad de Córdoba (BIO-276)
- Junta de Andalucía (BIO-276)
- National Institute on Aging
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics, phytochemicals, and oxidative stress
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Keywords
- Nrf2, gene deletion, cell immortalization, lifespan, murine embryonic fibroblasts, p53-dependent gene expression, cyclin E, NQO1, cytochrome b5 reductase, SIRT1, cellular aging, redox homeostasis, oxidative stress, oncogenes, carcinogenesis
- MeSH terms
- Animals, Fibroblasts, Gene Expression Regulation, Cellular Senescence, Sequence Deletion, NF-E2-Related Factor 2, Mice
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.
What counts as a claim ›How we measure confidence ›How we check this ›
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