Cited by 102Telomeres, Telomerase, and SenescenceGenetics, Aging, and Longevity in Model OrganismsCell death mechanisms and regulation

Chemotherapy-induced senescence, an adaptive mechanism driving resistance and tumor heterogeneity

Open access
Guillon, Jordan, Petit, Coralie, Toutain, Bertrand, Guette, Catherine, Lelièvre, Eric, Coqueret, Olivier·2019·Cell Cycle

Abstract

Senescence is activated in response to chemotherapy to prevent the propagation of cancer cells. In transformed cells, recent studies have shown that this response is not always definitive and that persistent populations can use senescence as an adaptive pathway to restart proliferation and become more aggressive. Here we discuss the results showing that an incomplete and heterogeneous senescence response plays a key role in chemotherapy resistance. Surviving to successive chemotherapy regimens, chronically existing senescent cells can create a survival niche through paracrine cooperations with neighboring cells. This favors chemotherapy escape of premalignant clones but might also allow the survival of adjacent clones presenting a lower fitness. A better characterization of senescence heterogeneity in transformed cells is therefore necessary. This will help us to understand this incomplete response to therapy and how it could generate clones with increased tumor capacity leading to disease relapse.

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Crossref · 10.1080/15384101.2019.1652047

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Authors
Guillon, J., Petit, C., Toutain, B., Guette, C., Lelièvre, E., & Coqueret, O.
Affiliations
Inserm (FR)
Corresponding author
Coqueret, Olivier
Venue
Cell Cycle
Published
2019-08-09
Volume
18
Issue
19
Pages
2385-2397
ISSN
  • 1538-4101 (ISSN-L)
  • 1551-4005
OpenAlex
W2966996218
Cited by
102
References
72
Citations by year
2026: 9 · 2025: 18 · 2024: 20 · 2023: 24 · 2022: 11 · 2021: 13 · 2020: 6 · 2019: 1
FWCI
0.91
Type
journal article
Language
en
Open access
Locations
  • Cell Cycle (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
  • HAL (submittedVersion)
Funders
Ligue Contre le Cancer (NA)
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
chemotherapy-induced senescence, chemoresistance, tumor heterogeneity, senescence escape, paracrine signaling, recurrence, senescent cells, tumor cell proliferation
MeSH terms
Antineoplastic Agents, Clone Cells, Humans, Neoplasm Recurrence, Local, Neoplasms, Signal Transduction, Oncogene Proteins, Gene Expression Regulation, Neoplastic, Cellular Senescence, Apoptosis, Drug Resistance, Neoplasm, Tumor Suppressor Proteins, Cell Proliferation

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