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Spontaneously slow-cycling subpopulations of human cells originate from activation of stress-response pathways

Min, Mingwei ; Spencer, Sabrina L Coller, Hilary A.

PLoS Biology, 2019-03, Vol.17 (3), p.e3000178 [Periódico revisado por pares]

United States: Public Library of Science

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Título:
Spontaneously slow-cycling subpopulations of human cells originate from activation of stress-response pathways
Autor: Min, Mingwei ; Spencer, Sabrina L
Coller, Hilary A.
Assuntos: Bacteria ; Biochemistry ; Bioinformatics ; Biology and Life Sciences ; Cell cycle ; Cell Cycle - genetics ; Cell Cycle - physiology ; Cell division ; Cell survival ; Cell Survival - genetics ; Cell Survival - physiology ; Cells (Biology) ; Cellular stress response ; Cycles ; Cyclin-dependent kinase 2 ; Cyclin-Dependent Kinase 2 - genetics ; Cyclin-Dependent Kinase 2 - metabolism ; Cyclin-dependent kinases ; Drug resistance ; Gene expression ; Gene sequencing ; Humans ; Kinases ; Metabolism ; Microbial colonies ; Neoplasms - metabolism ; Observations ; p53 Protein ; Physiological aspects ; Population ; Research and Analysis Methods ; Ribonucleic acid ; RNA ; RNA sequencing ; Signal Transduction - genetics ; Signal Transduction - physiology ; Stem cells ; Stress (Physiology) ; Subpopulations ; Survival ; Transcription ; Tumor proteins ; Yeast
É parte de: PLoS Biology, 2019-03, Vol.17 (3), p.e3000178
Notas: new_version
The authors have declared that no competing interests exist.
Descrição: 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.
Editor: United States: Public Library of Science
Idioma: Inglês

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Spontaneously slow-cycling subpopulations of human cells originate from activation of stress-response pathways

Min, Mingwei ; Spencer, Sabrina L Coller, Hilary A.

United States: Public Library of Science

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