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Murine fibroblasts lacking p21 undergo senescence and are resistant to transformation by oncogenic Ras.
Abstract
The cell-cycle inhibitor p21 is upregulated during senescence and upon induction of senescence-like arrest by oncogenic Ras. We have used primary fibroblasts derived from p21-null mice to evaluate the role of p21 in these processes. We find that primary p21-/- cells enter senescence and have a lifespan similar to wild-type cells. Upon immortalization, most wild-type and p21-/- cultures acquire alterations in either p53 or p16INK4a, further indicating that p21-deficiency is not sufficient by itself to allow immortalization. Primary p21-/- cells, like wild-type cells, respond to oncogenic Ras by accumulating p53 and p16INK4a, and by decreasing their proliferation rate. In agreement with this, p21-/- cells are refractory to neoplasic transformation by oncogenic Ras when compared to p53-/- cells. We conclude that, in murine fibroblasts, p21 is not essential neither for senescence nor for preventing neoplasic transformation by oncogenic Ras.
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“Increased expression of p21 also plays a role in induction of senescence, particularly during its initiation.26”
From Total body irradiation causes long-term mouse BM injury via induction of HSC premature senescence in an Ink4a- and Arf-independent manner (2014) · cites this paper as [26]
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SUMO-modified nuclear cyclin D1 bypasses Ras-induced senescence
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“Furthermore, genetic ablation of p21Cip1 in the mouse results in decreased DNA damage responses but not alter immortalization or susceptibility to Rasinduced transformation of primary fibroblasts (Brugarolas et al., 1995; Pantoja and Serrano, 1999).”
BackgroundInfluentialAP-1 dimers regulate transcription of the p14/p19ARF tumor suppressor gene
Ameyar‐Zazoua, M., Wisniewska, M. B., Bakiri, L., Wagner, E. F., Yaniv, M., & Weitzman, J. B. (2005) · Oncogene · doi:10.1038/sj.onc.1208424 · Cited by 42
“For example, ARF can induce cell-cycle arrest in mouse embryo fibroblasts (MEFs) lacking p21CIP1 or p53 (Pantoja and Serrano, 1999; Weber et al., 2000; Modestou et al., 2001).”
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Doumont, G., Martoriati, A., Beekman, C., Bogaerts, S., Mee, P. J., Bureau, F., Colombo, E., Alcalay, M., Bellefroid, E., Marchesi, F., et al. (2005) · The EMBO Journal · doi:10.1038/sj.emboj.7600769 · Cited by 40
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BackgroundInfluentialEssential role of the N-terminal region of TFII-I in viability and behavior
Lucena, J., Pezzi, S., Aso, E., Valero, M. C., Carreiro, C., Dubus, P. R., Sampaio, A., Puimedon, M. S., Barthelemy, I., Zindel, M. Y., et al. (2010) · BMC Medical Genetics · doi:10.1186/1471-2350-11-61 · Cited by 37
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Quantitative model of cell cycle arrest and cellular senescence in primary human fibroblasts
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“As expected (Harvey et al., 1993; Jones et al., 1996; Serrano et al., 1997; Pantoja and Serrano, 1999), p537/7 cells were able to form colonies with high e ciency whereas wild-type MEFs did not form any colonies (Table 2).”
BackgroundMethodInfluentialRegulation of the p53 pathway by Ras, the plot thickens
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“Total protein lysates were prepared as previously described (Pantoja and Serrano, 1999; Palmero et al., 2002).”
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Uekawa, N., Nishikimi, A., Isobe, K.-I., Iwakura, Y., & Maruyama, M. (2004) · FEBS Letters · doi:10.1016/j.febslet.2004.08.033 · Cited by 29
The role of p21 in regulating mammalian regeneration
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Pathway-specific effects of ADSL deficiency on neurodevelopment
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“The ΔPDL (difference in population doubling levels) was obtained by using the formula: log(N1/N0)/log2, where N1 is the number of cells at the timepoint we collected them and N0 is the initial number of cells plated ( Pantoja and Serrano, 1999 ).”
Novel ARF/p53-independent senescence pathways in cancer repression
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“However, p21-deficient MEFs undergo senescence and are resistant to Ras-induced transformation [72], suggesting that the role of p21 in cellular senescence may vary among species.”
BackgroundDGCR8-mediated disruption of miRNA biogenesis induces cellular senescence in primary fibroblasts
Gómez-Cabello, D., Adrados, I., Gamarra, D., Kobayashi, H., Takatsu, Y., Takatsu, K., Gil, J., & Palmero, I. (2013) · Aging Cell · doi:10.1111/acel.12117 · Cited by 26
“While this manuscript was in preparation, similar effects in tumor cell lines have been reported (Peric et al., 2012), in agreement with our work and in contrast to previous reports suggesting the opposite effect (Kumar et al., 2007).”
ResultEpimorphic regeneration in mice is p53-independent
Arthur, L. M., Demarest, R. M., Clark, L. D., Gourevitch, D., Bedelbaeva, K., Anderson, R., Snyder, A. R., Capobianco, A. J., Lieberman, P. M., Feigenbaum, L., et al. (2010) · Cell Cycle · doi:10.4161/cc.9.18.13119 · Cited by 25
Ing1 Mediates p53 Accumulation and Chromatin Modification in Response to Oncogenic Stress
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“For example, p21-deficient MEFs still undergo senescence (28), and a genetic interaction between p21 and pRb has not been examined in the setting of cellular senescence.”
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“MEFs with p21 loss of function show a delayed onset of senescence (Pantoja & Serrano, 1999), whereas human fibroblasts with p21 loss of function have been reported to completely bypass senescence (Brown et al, 1997).”
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“However, p21-null murine fibroblasts still undergo senescence, and they are resistant to transformation by ras (40).”
BackgroundSaleh, T., Khasawneh, A. I., Himsawi, N. M., Abu-Raideh, J. A., Ejeilat, V., Elshazly, A. M., & Gewirtz, D. A. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms232415512 · Cited by 21
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BackgroundHdmX overexpression inhibits oncogene induced cellular senescence
Miller, K. R., Kelley, K. D., Tuttle, R., & Berberich, S. J. (2010) · Cell Cycle · doi:10.4161/cc.9.16.12779 · Cited by 21
“For example, the inactivation of p21 by homologous recombination is sufficient to prevent senescence in human cells(10) while p21-null MEFs undergo senescence normally.(11) This difference implies that there is a missing link between the p53 and Rb pathways or other proteins can compensate for the loss of p21 in the m…”
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“The observation that deletion of the p21 gene does not result in increased spontaneous tumor development and can even decrease tumorigenesis (Pantoja and Serrano, 1999; Wang et al., 1997), suggests that p53 mutant alleles that retain some transactivation capability might confer a selectable…”
BackgroundMolecular mechanisms of cellular senescence and immortalization of human cells
Kiyono, T. (2007) · Expert Opinion on Therapeutic Targets · doi:10.1517/14728222.11.12.1623 · Cited by 16
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A ‘synthetic-sickness’ screen for senescence re-engagement targets in mutant cancer backgrounds
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“…and the role of some elements shown to induce senescence, such as telomere shortening (Chen et al., 2001; Munro et al., 2001; Von Zglinicki T, 2000), cell cycle inhibitors, tumor suppressors and oncogenes such as Ras, p21 and p14 (Chen et al., 2000b; Macip et al., 2002; Pantoja and Serrano, 1999).”
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“In contrast to p15 and p16, p21 is modestly induced, if at all, as MEFs are passaged in culture (10) and this is”
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BackgroundIdentification of the gene immediately downstream of the murine INK4a/ARF locus
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“Serial 3T3 cultivation was carried out essentially as described (see e.g., Pantoja and Serrano, 1999).”
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Metadata
- Authors
- Pantoja, C., & Serrano, M.
- Affiliations
- Consejo Superior de Investigaciones Científicas (ES)
- Venue
- Oncogene
- Published
- 1999-09-02
- Volume
- 18
- Issue
- 35
- Pages
- 4974-4982
- ISSN
- 0950-9232 (ISSN-L)
- 1476-5594
- OpenAlex
- W2081779271
- Cited by
- 201
- References
- 78
- Citations by year
- 2025: 3 · 2023: 6 · 2022: 4 · 2021: 1 · 2020: 4 · 2019: 3 · 2018: 3 · 2017: 4 · 2016: 6 · 2015: 7 · 2014: 7 · 2013: 11 · 2012: 6
- FWCI
- 8.20
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Oncogene (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Telomeres, Telomerase, and Senescence
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Keywords
- p21, cellular senescence, oncogenic Ras, oncogenic transformation, p53, p16INK4a, cell cycle inhibitors, fibroblasts, cell immortalization
- MeSH terms
- Animals, Cell Cycle, Cell Division, Cell Line, Transformed, Cell Transformation, Neoplastic, Cells, Cultured, Doxorubicin, Fibroblasts, Serial Passage, Transduction, Genetic, Oncogene Protein p21(ras), Gene Expression, Tumor Suppressor Protein p53, Cyclins, 3T3 Cells, Cellular Senescence, Gene Deletion, Mice, Knockout, Cyclin-Dependent Kinase Inhibitor p16, Cyclin-Dependent Kinase Inhibitor p21, Mice
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