Cited by 255Telomeres, Telomerase, and SenescenceTGF-β signaling in diseasesCancer Cells and Metastasis

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Epithelial-Mesenchymal Transition Induced by Senescent Fibroblasts

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Laberge, Remi-Martin, Awad, Pierre, Campisi, Judith, Desprez, Pierre-Yves·2012·Cancer Microenvironment

DOI 10.1007/s12307-011-0069-4PMC PMC3343197

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Abstract

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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Authors: Laberge, R.-M., Awad, P., Campisi, J., & Desprez, P.-Y.
Affiliations: Buck Institute for Research on Aging (US)
Corresponding author: Desprez, Pierre-Yves
ORCID: Campisi, Judith
Desprez, Pierre-Yves
Venue: Cancer Microenvironment
Publisher: Springer Science and Business Media LLC
Published: 2011-06-25
Volume: 5
Issue: 1
Pages: 39-44
ISSN: 1875-2284 (ISSN-L)
1875-2292
DOI: 10.1007/s12307-011-0069-4
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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Epithelial-Mesenchymal Transition Induced by Senescent Fibroblasts

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