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

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Cellular senescence: putting the paradoxes in perspective

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

DOI 10.1016/j.gde.2010.10.005PMC PMC3073609

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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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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)
DOI: 10.1016/j.gde.2010.10.005
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
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/legal/tdmrep-license (tdm)
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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Cellular senescence: putting the paradoxes in perspective

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