ATRX is a regulator of therapy induced senescence in human cells
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Senescence is a state of stable cell cycle exit with important implications for development and disease. Here, we demonstrate that the chromatin remodeling enzyme ATRX is required for therapy-induced senescence. ATRX accumulates in nuclear foci and is required for therapy-induced senescence in multiple types of transformed cells exposed to either DNA damaging agents or CDK4 inhibitors. Mobilization into foci depends on the ability of ATRX to interact with H3K9me3 histone and HP1. Foci form soon after cells exit the cell cycle, before other hallmarks of senescence appear. Eliminating ATRX in senescent cells destabilizes the senescence-associated heterochromatic foci. Additionally, ATRX binds to and suppresses expression from the HRAS locus; repression of HRAS is sufficient to promote the transition of quiescent cells into senescence and preventing repression blocks progression into senescence. Thus ATRX is a critical regulator of therapy-induced senescence and acts in multiple ways to drive cells into this state.Therapy induced senescence (TIS) is a growth suppressive program activated by cytostatic agents in some cancer cells. Here the authors show that the chromatin remodeling enzyme ATRX is a regulator of TIS and drives cells into this state via multiple mechanisms.
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Down-regulation of MDM2, redistribution of ATRX, and repression of HRAS transcription are necessary for the transition from CDK4 inhibitor-induced quiescence to senescence in several mesenchymal and epithelial tumor cell lines.
“Specifically, down-regulation of MDM2, redistribution of the chromatin remodeling enzyme ATRX, and repression of HRAS transcription are necessary for the transition of CDK4 inhibitor-induced quiescence into senescence in a number of mesenchymal and epithelial cell lines derived from different tumor types, including breast, non-small cell lung cancer, soft tissue sarcoma and glioma (Kovatcheva et a”
From CDK4/6 Inhibitors: The Mechanism of Action May Not Be as Simple as Once Thought (2018) · cites this paper as Kovatcheva et al., 2017
Quiescent CDK4/6 inhibitor-arrested liposarcoma cells are pushed into senescence by HRAS knockdown, and near-physiologic HRAS mRNA expression prevents senescence after CDK4/6 inhibition while cells still exit the cell cycle.
“Indeed, quiescent CDK4/6 inhibitor arrested liposarcoma tumor cells are pushed into senescence upon knocking down HRAS, and enforced expression of near physiologic levels of HRAS mRNA is able to prevent cells from undergoing senescence following treatment with CDK4/6 inhibitors albeit they still exit the cell cycle (Kovatcheva 2017).”
From CDK4/6 Inhibitors: The Mechanism of Action May Not Be as Simple as Once Thought (2018) · cites this paper as Kovatcheva 2017
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- Authors
- Kovatcheva, M., Liao, W., Klein, M. E., Robine, N., Geiger, H., Crago, A. M., Dickson, M. A., Tap, W. D., Singer, S., & Koff, A.
- Affiliations
- Memorial Sloan Kettering Cancer Center (US)
- New York Genome Center (US)
- Corresponding author
- Koff, Andrew
- ORCID
- Venue
- Nature Communications
- Published
- 2017-08-30
- Volume
- 8
- Issue
- 1
- Pages
- 386-386
- ISSN
- 2041-1723 (ISSN-L)
- PMC
- PMC5577318
- OpenAlex
- W2748768502
- Cited by
- 89
- References
- 73
- Citations by year
- 2026: 5 · 2025: 17 · 2024: 7 · 2023: 10 · 2022: 6 · 2021: 10 · 2020: 17 · 2019: 7 · 2018: 8 · 2017: 2
- FWCI
- 6.88
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Nature Communications (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Sarcoma Foundation of America
- Cycle for Survival (P30 CA008748)
- National Institutes of Health (CA008748, NIH/NCI Cancer Center Support Grant P30 CA008748)
- National Cancer Institute (Grant P30-CA008748, CA008748, NIH/NCI Cancer Center Support Grant P30 CA008748., P50CA140146, Support Grant P30 CA008748, CA140146, P30CA008748)
- Topics
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Keywords
- ATRX, therapy-induced senescence, cellular senescence, chromatin remodeling, H3K9me3, HP1, senescence-associated heterochromatin foci, CDK4 inhibitors, DNA damage, cell cycle exit, transformed cells
- MeSH terms
- X-linked Nuclear Protein, Cell Cycle, Chromatin, DNA Damage, Heterochromatin, Histones, Humans, RNA, Messenger, Cellular Senescence, Cell Line, Tumor, Protein Kinase Inhibitors, Cell Proliferation
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