Stress-induced cellular senescence contributes to chronic inflammation and cancer progression.
Open accessAbstract
Cellular senescence has long been considered to act as a tumor suppressor or tumor suppression mechanism and described as a phenomenon of irreversible cell cycle arrest. Cellular senescence, however, is now considered to have physiological functions other than tumor suppression; it has been found to be involved in embryogenesis, tissue/organ aging, and wound healing. Surprisingly, cellular senescence is also demonstrated to have a tumor progressive role in certain situations. Senescent cells exhibit secretory phenotypes called senescence-associated secretory phenotype (SASP), which secrete a variety of SASP factors including inflammatory cytokines, chemokines, and growth factors, as well as matrix remodeling factors that promote the alteration of neighboring tissue microenvironments. Such SASP factors have been known to drive the mechanisms underlying the pleiotropic features of cellular senescence. In this review, we examine current knowledge of cellular senescence at molecular and cellular levels, with a focus on chronic inflammation and tumor progression.
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Activation of p53/p21WAF1/CIP1 and p16INK4A/pRB tumor suppressor pathways plays a central role in regulating senescence.
“Activation of the p53/p21WAF1/CIP1 and p16INK4A/pRB tumor suppressor pathways play a central role in regulating senescence.”
From Mechanisms of Cellular Senescence: Cell Cycle Arrest and Senescence Associated Secretory Phenotype (2021) · cites this paper as Kobashigawa et al., 2019
Cell cycle arrest in senescence is largely mediated via activation of either one or both p53/p21WAF1/CIP1 and p16INK4A/pRB tumor suppressor pathways.
“Cell cycle arrest in senescence is largely mediated via activation of either one or both p53/p21WAF1/CIP1 and p16INK4A/pRB tumor suppressor pathways (Rovillain et al., 2011; Kobashigawa et al., 2019; Liu and Wan, 2019).”
From Mechanisms of Cellular Senescence: Cell Cycle Arrest and Senescence Associated Secretory Phenotype (2021) · cites this paper as Kobashigawa et al., 2019
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References 124 · Cited by 18
- Authors
- KOBASHIGAWA, S., M. SAKAGUCHI, Y., MASUNAGA, S., & MORI, E.
- Affiliations
- Kyoto University (JP)
- Department of Future Basic Medicine, Nara Medical University
- Kyoto University, Institute of Integrated Radiation and Nuclear Science
- Nara Medical University (JP)
- Venue
- Thermal Medicine
- Published
- 2019-12-15
- Volume
- 35
- Issue
- 4
- Pages
- 41-58
- ISSN
- 1882-2576 (ISSN-L)
- 1882-3750
- OpenAlex
- W3002328327
- Cited by
- 18
- References
- 124
- Citations by year
- 2026: 5 · 2025: 3 · 2024: 3 · 2022: 4 · 2021: 2 · 2020: 1
- FWCI
- 1.20
- Type
- journal article
- Language
- en
- Open access
- diamond
- doi.org
- Locations
- Thermal Medicine (publishedVersion)
- Funders
- Konica Minolta Imaging Science Foundation
- Nakatomi Foundation
- Nara Medical University
- Mochida Memorial Foundation for Medical and Pharmaceutical Research
- SENSHIN Medical Research Foundation
- Terumo Foundation for Life Sciences and Arts
- Japan Society for the Promotion of Science (19K08171, 19K08150, 16K19836, 17H07031)
- 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 › Geriatrics and Gerontology › Sirtuins and Resveratrol in Medicine
- Keywords
- cellular senescence, senescence-associated secretory phenotype, chronic inflammation, tumor progression, tumor suppression, inflammatory cytokines, chemokines, extracellular matrix remodeling, tumor microenvironment, stress-induced senescence
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