ArticlePhysical biology2013
Modulating cell-to-cell variability and sensitivity to death ligands by co-drugging.
Article in Physical biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed.
- Evasion of cell death despite mitochondrial outer membrane permeabilization: an oncogenic outcome of apoptosis.Apoptosis : an international journal on programmed cell death · 2026Review
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- TRAIL signaling promotes entosis in colorectal cancer.The Journal of cell biology · 2021Article
- Novel Apoptosis-Inducing Agents for the Treatment of Cancer, a New Arsenal in the Toolbox.Cancers · 2019Review
- Quantitative single cell analysis uncovers the life/death decision in CD95 network.PLoS computational biology · 2018Article
- Microenvironmental Signals and Biochemical Information Processing: Cooperative Determinants of Intratumoral Plasticity and Heterogeneity.Frontiers in cell and developmental biology · 2018Review
- Reciprocal amplification of caspase-3 activity by nuclear export of a putative human RNA-modifying protein, PUS10 during TRAIL-induced apoptosis.Cell death & disease · 2017Article
- The recurrent architecture of tumour initiation, progression and drug sensitivity.Nature reviews. Cancer · 2017Review
- Article
- A passive-flow microfluidic device for imaging latent HIV activation dynamics in single T cells.Integrative biology : quantitative biosciences from nano to macro · 2015Article
- Surviving apoptosis: life-death signaling in single cells.Trends in cell biology · 2015Review
- Modeling dynamics of cell-to-cell variability in TRAIL-induced apoptosis explains fractional killing and predicts reversible resistance.PLoS computational biology · 2014Article
- Mass cytometry to decipher the mechanism of nongenetic drug resistance in cancer.Current topics in microbiology and immunology · 2014Review
- Cells surviving fractional killing by TRAIL exhibit transient but sustainable resistance and inflammatory phenotypes.Molecular biology of the cell · 2013Article
- Determinants of cell-to-cell variability in protein kinase signaling.PLoS computational biology · 2013Article
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
TRAIL (tumor necrosis factor-related apoptosis-inducing ligand) holds promise as an anti-cancer therapeutic but efficiently induces apoptosis in only a subset of tumor cell lines. Moreover, even in clonal populations of responsive lines, only a fraction of cells dies in response to TRAIL and individual cells exhibit cell-to-cell variability in the timing of cell death. Fractional killing in these cell populations appears to arise not from genetic differences among cells but rather from differences in gene expression states, fluctuations in protein levels and the extent to which TRAIL-induced death or survival pathways become activated. In this study, we ask how cell-to-cell variability manifests in cell types with different sensitivities to TRAIL, as well as how it changes when cells are exposed to combinations of drugs. We show that individual cells that survive treatment with TRAIL can regenerate the sensitivity and death-time distribution of the parental population, demonstrating that fractional killing is a stable property of cell populations. We also show that cell-to-cell variability in the timing and probability of apoptosis in response to treatment can be tuned using combinations of drugs that together increase apoptotic sensitivity compared to treatment with one drug alone. In the case of TRAIL, modulation of cell-to-cell variability by co-drugging appears to involve a reduction in the threshold for mitochondrial outer membrane permeabilization.
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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.