ArticlePLoS biology2019
Spontaneously slow-cycling subpopulations of human cells originate from activation of stress-response pathways.
Article in PLoS biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 1 of them a synthesis that pooled it.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
57 citing papers in PubMed, 1 synthesis or guideline pooled it, 96 citations in OpenAlex.
- "Quiescence" in the resting zone of the growth plate: a systematic review.Stem cells (Dayton, Ohio) · 2026Pooled it
- Spatial ecology of breast cancer reveals co-evolution of proliferative and dormant niches.Genome medicine · 2026Article
- The dynamics of centromere assembly and disassembly during quiescence.The Journal of cell biology · 2026Article
- G0 or no-G0: phosphatase control of quiescence and cell cycle entry.Biochemical Society transactions · 2026Review
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- Single cell snapshot analyses under proper representation reveal that epithelial-mesenchymal transition couples at G1 and G2/M.Communications biology · 2026Article
- Drug-tolerant persister cells in cancer: bridging the gaps between bench and bedside.Nature communications · 2025Review
- Stress granules promote quiescence by enhancing p21 levels and reducing phospho-Rb.RNA (New York, N.Y.) · 2025Article
- The dynamics of centromere assembly and disassembly during quiescence.bioRxiv : the preprint server for biology · 2025Article
- Exploring the Single-Cell Dynamics of FOXM1 Under Cell Cycle Perturbations.Cell proliferation · 2025Article
- Mechanistic modeling of cell viability assays with in silico lineage tracing.PLoS computational biology · 2025Article
- Reversible proliferative arrest induced by rapid depletion of RNase MRP.Nature communications · 2025Article
- Inferring metabolic objectives and trade-offs in single cells during embryogenesis.Cell systems · 2025Article
- Transcription factor networks in cellular quiescence.Nature cell biology · 2025Review
- SynonymousNAR genomics and bioinformatics · 2024Article
- Targeting therapy-persistent residual disease.Nature cancer · 2024Review
- Memory loss and aberrant neurogenesis in mice exposed to patient anti-N-methyl-d-aspartate receptor antibodies.Experimental neurology · 2024Article
- Low-frequency ERK and Akt activity dynamics are predictive of stochastic cell division events.NPJ systems biology and applications · 2024Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Slow-cycling subpopulations exist in bacteria, yeast, and mammalian systems. In the case of cancer, slow-cycling subpopulations have been proposed to give rise to drug resistance. However, the origin of slow-cycling human cells is poorly studied, in large part due to lack of markers to identify these rare cells. Slow-cycling cells pass through a noncycling period marked by low CDK2 activity and high p21 levels. Here, we use this knowledge to isolate these naturally slow-cycling cells from a heterogeneous population and perform RNA sequencing to delineate the transcriptome underlying the slow-cycling state. We show that cellular stress responses-the p53 transcriptional response and the integrated stress response (ISR)-are the most salient causes of spontaneous entry into the slow-cycling state. Finally, we show that cells' ability to enter the slow-cycling state enhances their survival in stressful conditions. Thus, the slow-cycling state is hardwired to stress responses to promote cellular survival in unpredictable environments.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.