Senescence and the Pro-tumorigenic Stroma
Open accessAbstract
Hayflick and Moorhead first described senescence in the late 1960's as a permanent growth arrest that primary cells underwent after a defined number of cellular divisions in culture. This observation gave rise to the hypothesis that cells contained an internal counting mechanism that limited cellular division and that this limit was an important barrier to cellular transformation. What began as an in vitro observation has led to an immense body of work that reaches into all fields of biology and is of particular interest in the areas of aging, tissue regeneration, and tumorigenesis. The initially simplistic view that senescence limits cellular division and contributes to aging while stymying tumorigenesis has now evolved into an important and complex biological process that has numerous caveats and often opposing effects on tumorigenesis. In this review, we limit our discussion to the complex role senescence plays in tumorigenesis. Throughout the review we attempt to draw many parallels to other systems including the role senescent cells play in the tumor microenvironment and their significant molecular and phenotypic similarities to cancer associated fibroblasts (CAFs).
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Cells present in the tumour microenvironment, such as fibroblasts, can become senescent and promote the growth and proliferation of tumour cells.
“Cells present in the tumour microenvironment, such as fibroblasts, can become senescent and promote the growth and proliferation of tumour cells.7,39,40”
From Paracrine roles of cellular senescence in promoting tumourigenesis (2018) · cites this paper as [39]
Senescent cells can contribute to the acquisition of invasive and metastatic properties of cancer cells, as well as the induction of tumour-associated angiogenesis.
“Senescent cells can contribute to the acquisition of invasive and metastatic properties of cancer cells, as well as the induction of tumour-associated angiogenesis.7,39”
From Paracrine roles of cellular senescence in promoting tumourigenesis (2018) · cites this paper as [39]
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References 67 · Cited by 47
- Authors
- Alspach, E., Fu, Y., & Stewart, S. A.
- Affiliations
- Washington University in St. Louis (US)
- Corresponding author
- Stewart, Sheila A.
- Venue
- Critical Reviews in Oncogenesis
- Publisher
- Begell House
- Published
- 2013
- Volume
- 18
- Issue
- 6
- Pages
- 549-558
- ISSN
- 0893-9675 (ISSN-L)
- PMC
- PMC3951899
- OpenAlex
- W2082089719
- Cited by
- 47
- References
- 67
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 1 · 2023: 2 · 2022: 7 · 2021: 6 · 2020: 10 · 2019: 5 · 2018: 4 · 2017: 2 · 2016: 1 · 2015: 5 · 2014: 1
- FWCI
- 1.62
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Locations
- Critical Reviews™ in Oncogenesis (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Cancer Institute (R01CA130919)
- National Institute of General Medical Sciences (T32GM007067)
- Topics
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › TGF-β signaling in diseases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Keywords
- cellular senescence, carcinogenesis, tumor microenvironment, cancer-associated fibroblasts, senescence-associated secretory phenotype, growth arrest, aging, tissue regeneration, cell transformation
- MeSH terms
- Animals, DNA Damage, Humans, Biomarkers, Cellular Senescence, Carcinogenesis, Ataxia Telangiectasia Mutated Proteins
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