The DOI matches its Crossref record; 65 of the 65 references it cites were found in a registry or an index.
Epithelial-Mesenchymal Transition Induced by Senescent Fibroblasts
Open accessAbstract
Depending on the cell type and tissue environment, epithelial and mesenchymal cell phenotypes are not static and can be highly dynamic. Epithelial-mesenchymal transitions (EMTs) and reverse EMTs provide flexibility during embryogenesis. While EMTs are a critical normal process during development and wound healing, properties of the EMT have been implicated in human pathology, particularly cancer metastasis. A normal undamaged epithelium does not typically exhibit features of an EMT. However, particularly under the influence of the surrounding microenvironment, cancer cells may reactivate developmental phenotypes out of context in the adult. This reactivation, such as the EMT, can facilitate tumor cell invasion and metastasis, and therefore is a major mechanism of tumor progression. Conversely, cellular senescence, which is associated with aging, is a process by which cells enter a state of permanent cell cycle arrest, thereby constituting a potent tumor suppressive mechanism. However, accumulating evidence shows that senescent cells can have deleterious effects on the tissue microenvironment. The most significant of these effects is the acquisition of a senescence-associated secretory phenotype (SASP) that turns senescent fibroblasts into pro-inflammatory cells having the ability to promote tumor progression, in part by inducing an EMT in nearby epithelial cells. Here, we summarize the potential impacts of SASP factors, particularly interleukins, on tissue microenvironments and their ability to stimulate tumor progression through induction of an EMT.
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“Senescent fibroblasts induce an epithelial-to-mesenchymal transition in premalignant epithelial cells and nonaggressive cancer epithelial cells in part through the secretion of IL-6 and IL-8 (32, 102, 118).”
From Aging, Cellular Senescence, and Cancer (2013) · cites this paper as [102]
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“In addition to stimulating tumor growth in mice, SASP factors can stimulate malignant phenotypes in culture.”
From Aging, Cellular Senescence, and Cancer (2013) · cites this paper as [102]
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“One such phenotype is the epithelial-to-mesenchymal transition (102) (Figure 2).”
From Aging, Cellular Senescence, and Cancer (2013) · cites this paper as [102]
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“The SASP can have a major impact on various biological processes, including cell proliferation, angiogenesis, inflammation16, epithelial-to-mesenchymal transition17, tissue repair18 and wound healing3 (Fig. 2).”
From Spatial mapping of cellular senescence: emerging challenges and opportunities (2023) · cites this paper as [17]
In the citing paper
“A known pathway for SASP-promoted cancer metastasis is the induction of epithelial to mesenchymal transition (EMT)”
From Redox control of senescence and age-related disease. (2017) · cites this paper as [106]
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Citations
Cites
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The basics of epithelial-mesenchymal transition
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Thiery, J. P. (2002) · Nature reviews. Cancer · doi:10.1038/nrc822 · Cited by 6,767
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Hayflick, L. (1965) · Experimental Cell Research · doi:10.1016/0014-4827(65)90211-9 · Cited by 5,876
The senescence-associated secretory phenotype: the dark side of tumor suppression
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Self-citationCellular senescence: when bad things happen to good cells
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Self-citationA DNA damage checkpoint response in telomere-initiated senescence
Fagagna, F. D. D., Reaper, P. M., Clay-Farrace, L., Fiegler, H., Carr, P., von Zglinicki, T., Saretzki, G., Carter, N. P., & Jackson, S. P. (2003) · Nature · doi:10.1038/nature02118 · Cited by 2,917 · cited 1×
“damage signal that permanently arrests growth [15].”
Met, metastasis, motility and more
Birchmeier, C., Birchmeier, W., Gherardi, E., & Woude, G. F. V. (2003) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm1261 · Cited by 2,652
Cited by
Sorted by citations
Oxidative stress, aging, and diseases
Liguori, I., Russo, G., Curcio, F., Bulli, G., Aran, L., Della-Morte, D., Gargiulo, G., Testa, G., Cacciatore, F., Bonaduce, D., et al. (2018) · Clinical Interventions in Aging · doi:10.2147/cia.s158513 · Cited by 3,979
Aging, Cellular Senescence, and Cancer
Campisi, J. (2013) · Annual Review of Physiology · doi:10.1146/annurev-physiol-030212-183653 · Cited by 2,954
Self-citationThe role of senescent cells in ageing
van Deursen, J. M. (2014) · Nature · doi:10.1038/nature13193 · Cited by 2,623
Kastenhuber, E. R., & Lowe, S. W. (2017) · Cell · doi:10.1016/j.cell.2017.08.028 · Cited by 1,906
Epithelial-Mesenchymal Transition in Cancer: A Historical Overview
Ribatti, D., Tamma, R., & Annese, T. (2020) · Translational Oncology · doi:10.1016/j.tranon.2020.100773 · Cited by 1,051
Metadata
- Authors
- Laberge, R.-M., Awad, P., Campisi, J., & Desprez, P.-Y.
- Affiliations
- Buck Institute for Research on Aging (US)
- Corresponding author
- Desprez, Pierre-Yves
- Venue
- Cancer Microenvironment
- Published
- 2011-06-25
- Volume
- 5
- Issue
- 1
- Pages
- 39-44
- ISSN
- 1875-2284 (ISSN-L)
- 1875-2292
- PMC
- PMC3343197
- OpenAlex
- W2083594352
- Cited by
- 255
- References
- 65
- Citations by year
- 2026: 11 · 2025: 14 · 2024: 26 · 2023: 20 · 2022: 17 · 2021: 20 · 2020: 22 · 2019: 15 · 2018: 20 · 2017: 24 · 2016: 13 · 2015: 12 · 2014: 15 · 2013: 14 · 2012: 9
- FWCI
- 8.95
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Cancer Microenvironment (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › TGF-β signaling in diseases
- Health Sciences › Medicine › Oncology › Cancer Cells and Metastasis
- Keywords
- epithelial-mesenchymal transition, cellular senescence, senescence-associated secretory phenotype, senescent fibroblasts, tumor progression, metastasis, tumor microenvironment, interleukins, tumor invasion
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