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Cellular senescence: putting the paradoxes in perspective
Open accessAbstract
Cellular senescence arrests the proliferation of potential cancer cells, and so is a potent tumor suppressive mechanism, akin to apoptosis. Or is it? Why did cells evolve an anti-cancer mechanism that arrests, rather than kills, would-be tumor cells? Recent discoveries that senescent cells secrete growth factors, proteases and cytokines provide a shifting view--from senescence as a cell autonomous suppressor of tumorigenesis to senescence as a means to mobilize the systemic and local tissue milieu for repair. In some instances, this mobilization benefits the organism, but in others it can be detrimental. These discoveries provide potential mechanisms by which cellular senescence might contribute to the diverse, and seemingly incongruent, processes of tumor suppression, tumor promotion, tissue repair, and aging.
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“Recent findings have uncovered an additional beneficial effect of the senescence response and accompanying SASP: the ability to promote optimal repair of damaged tissue (59, 91, 145–147).”
From Aging, Cellular Senescence, and Cancer (2013) · cites this paper as [145]
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“Cellular senescence, which halts the proliferation of damaged or dysfunctional cells, is an important mechanism to constrain the malignant progression of tumour cells1,2.”
From Clearance of p16Ink4a-positive senescent cells delays ageing-associated disorders (2011) · cites this paper as [1]
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Sorted by citations
Clearance of p16Ink4a-positive senescent cells delays ageing-associated disorders
Baker, D. J., Wijshake, T., Tchkonia, T., LeBrasseur, N. K., Childs, B. G., van de Sluis, B., Kirkland, J. L., & van Deursen, J. M. (2011) · Nature · doi:10.1038/nature10600 · Cited by 3,670
“Cellular senescence, which halts the proliferation of damaged or dysfunctional cells, is an important mechanism to constrain the malignant progression of tumour cell”
Aging, Cellular Senescence, and Cancer
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Metadata
- Authors
- Campisi, J.
- Affiliations
- Buck Institute for Research on Aging (US)
- Corresponding author
- Campisi, Judith
- ORCID
- Campisi, Judith
- Venue
- Current Opinion in Genetics & Development
- Publisher
- Elsevier BV
- Published
- 2011-02
- Volume
- 21
- Issue
- 1
- Pages
- 107-112
- ISSN
- 0959-437X (ISSN-L)
- PMC
- PMC3073609
- OpenAlex
- W2027082499
- Cited by
- 368
- References
- 48
- Citations by year
- 2026: 15 · 2025: 19 · 2024: 13 · 2023: 14 · 2022: 13 · 2021: 17 · 2020: 26 · 2019: 30 · 2018: 15 · 2017: 22 · 2016: 27 · 2015: 33 · 2014: 30 · 2013: 39 · 2012: 31
- FWCI
- 3.02
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Current Opinion in Genetics & Development (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Science Foundation
- American Federation for Aging Research
- KWF Kankerbestrijding
- National Institutes of Health
- National Institute on Aging (RL1AG032117, P01AG025901, R37AG009909, P01AG017242, R01AG034421, T32AG000266)
- National Institute of Environmental Health Sciences (RL1ES016655)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › 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 › TGF-β signaling in diseases
- Keywords
- cellular senescence, tumor suppression, senescence-associated secretory phenotype, tissue repair, aging, tumor promotion
- MeSH terms
- Animals, Humans, Neoplasms, Phenotype, Cellular Senescence, Disease Progression
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