Cited by 368Telomeres, Telomerase, and SenescenceGenetics, Aging, and Longevity in Model OrganismsTGF-β signaling in diseases

Cellular senescence: putting the paradoxes in perspective

Open access
Campisi, Judith·2011·Current Opinion in Genetics & Development

Abstract

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.

    “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]

  • Cellular senescence halts proliferation of damaged or dysfunctional cells and constrains malignant progression of tumour cells.

    “Cellular senescence, which halts the proliferation of damaged or dysfunctional cells, is an important mechanism to constrain the malignant progression of tumour cells1,2.”

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Authors
Campisi, J.
Affiliations
Buck Institute for Research on Aging (US)
Corresponding author
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)
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
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
  • 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 › 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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