Cited by 57Telomeres, Telomerase, and SenescenceGenetics, Aging, and Longevity in Model OrganismsCancer-related Molecular Pathways

Cellular senescence: a double‐edged sword in the fight against cancer

Ohtani, Naoko, Takahashi, Akiko, Mann, David J., Hara, Eiji·2012·Experimental Dermatology

Abstract

Over the last few decades, it has become apparent that oncogenic proliferative signals are coupled to a variety of growth inhibitory responses, such as the induction of apoptotic cell death or irreversible cell cycle arrest known as 'cellular senescence'. Thus, both apoptosis and cellular senescence are thought to act as important tumor suppression mechanisms. Unlike apoptotic cells, however, senescent cells remain viable for long periods of time and accumulate with increasing age in various organs and tissues. Moreover, recent studies reveal that although cellular senescence initially functions as a tumor suppressive process, it may eventually exhibit tumor-promoting effects. Therefore, it is conceivable that accumulation of senescent cells during the ageing process in vivo may contribute to the age-related increase in cancer incidence. In this review, we provide an update and perspective on recent advances made in understanding the deleterious side effects of cellular senescence.

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Crossref · 10.1111/j.1600-0625.2012.01493.x

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67 of 67 references verified0 citation errors · 0 not checkable

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  • Senescent cells express the SASP, a cell-type and signal-specific program of gene expression and cytokine secretion that can sculpt the immune response.

    “Senescent cells express a cell type and signal specific program of gene expression and cytokine secretion (the SASP), which can sculpt the immune response (Ohtani et al., 2012).”

    From CDK4/6 Inhibitors: The Mechanism of Action May Not Be as Simple as Once Thought (2018) · cites this paper as Ohtani et al., 2012

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Authors
Ohtani, N., Takahashi, A., Mann, D. J., & Hara, E.
Affiliations
  • Japan Science and Technology Agency (JP)
  • Japanese Foundation For Cancer Research (JP)
  • Imperial College London (GB)
Corresponding author
Hara, Eiji
Venue
Experimental Dermatology
Publisher
Wiley
Published
2012-05-24
Volume
21
Issue
s1
Pages
1-4
ISSN
  • 0906-6705 (ISSN-L)
  • 1600-0625
OpenAlex
W2163432085
Cited by
57
References
66
Citations by year
2026: 1 · 2025: 3 · 2024: 2 · 2022: 7 · 2021: 8 · 2020: 3 · 2019: 1 · 2018: 7 · 2017: 2 · 2016: 7 · 2015: 6 · 2014: 3 · 2013: 6 · 2012: 1
FWCI
0.55
Type
journal article
Language
en
Open access
closed
Locations
  • Experimental Dermatology (publishedVersion)
  • PubMed (publishedVersion)
Funders
Japan Science and Technology Agency
Topics
  • Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
  • Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
Keywords
cellular senescence, tumor suppression, apoptosis, tumor promotion, senescence-associated secretory phenotype, aging, age-related cancer incidence, cell cycle arrest
MeSH terms
Animals, Cell Transformation, Neoplastic, DNA Damage, Humans, Inflammation, Models, Biological, Neoplasms, Gene Expression Regulation, Neoplastic, Genes, Tumor Suppressor, Cellular Senescence, Apoptosis, Oxidative Stress, Epigenesis, Genetic, Cell Proliferation

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