Regulation of senescence escape by TSP1 and CD47 following chemotherapy treatment
Open accessAbstract
Senescence is a tumor-suppressive mechanism induced by telomere shortening, oncogenes, or chemotherapy treatment. Although it is clear that this suppressive pathway leads to a permanent arrest in primary cells, this might not be the case in cancer cells that have inactivated their suppressive pathways. We have recently shown that subpopulations of cells can escape chemotherapy-mediated senescence and emerge as more transformed cells that induce tumor formation, resist anoikis, and are more invasive. In this study, we characterized this emergence and showed that senescent cells favor tumor growth and metastasis, in vitro and in vivo. Senescence escape was regulated by secreted proteins produced during emergence. Among these, we identified thrombospondin-1 (TSP1), a protein produced by senescent cells that prevented senescence escape. Using SWATH quantitative proteomic analysis, we found that TSP1 can be detected in the serum of patients suffering from triple-negative breast cancer and that its low expression was associated with treatment failure. The results also indicate that senescence escape is explained by the emergence of CD47 low cells that express a reduced level of CD47, the TSP1 receptor. The results show that CD47 expression is regulated by p21waf1. The cell cycle inhibitor was sufficient to maintain senescence since its downregulation in senescent cells increased cell emergence. This leads to the upregulation of Myc, which then binds to the CD47 promoter to repress its expression, allowing the generation of CD47 low cells that escape the suppressive arrest. Altogether, these results uncovered a new function for TSP1 and CD47 in the control of chemotherapy-mediated senescence.
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The increased signaling through ECM-related pathways highlights extensive ECM remodeling within the senescent microenvironment.
“The increased signaling through these ECM-related pathways highlights extensive ECM remodeling within the senescent microenvironment.52,53”
From Cellular senescence in human liver under normal aging and cancer (2026) · cites this paper as [52]
The Results section on thrombospondin-1 reports increased MMP expression in emergent cells and increased secretion of TSP1 by senescent cells. The paper does not report increased signaling across ECM-related pathways or demonstrate extensive ECM remodeling in the senescent microenvironment. Page numbers are unavailable in our copy. (LLM, conf=0.76)
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- Authors
- Guillon, J., Petit, C., Moreau, M., Toutain, B., Henry, C., Roché, H., Bonichon-Lamichhane, N., Salmon, J. P., Lemonnier, J., Campone, M., Verrièle, V., Lelièvre, E., Guette, C., & Coqueret, O.
- Affiliations
- Inserm (FR)
- Institut universitaire du cancer de Toulouse Oncopole (FR)
- CHR Verviers (BE)
- UniCancer Group (FR)
- Corresponding author
- Coqueret, Olivier
- ORCID
- Venue
- Cell Death & Disease
- Published
- 2019-02-27
- Volume
- 10
- Issue
- 3
- Pages
- 199-199
- ISSN
- 2041-4889 (ISSN-L)
- PMC
- PMC6393582
- OpenAlex
- W2917200827
- Cited by
- 90
- References
- 29
- Citations by year
- 2026: 8 · 2025: 8 · 2024: 13 · 2023: 17 · 2022: 9 · 2021: 19 · 2020: 7 · 2019: 7 · 2015: 1
- FWCI
- 7.20
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Cell Death and Disease (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, other-oa)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- HAL (submittedVersion, other-oa)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Funders
- Ligue Contre le Cancer
- Fondation de France
- Topics
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Keywords
- senescence escape, chemotherapy-induced senescence, thrombospondin-1, CD47, p21, c-Myc, triple-negative breast cancer, tumor growth, metastasis, anoikis resistance, cell invasion, treatment failure, secreted proteins
- MeSH terms
- Animals, Humans, Cellular Senescence, Thrombospondin 1, Mice, CD47 Antigen
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