ArticlePLoS computational biology2020
A mechanism for epithelial-mesenchymal heterogeneity in a population of cancer cells.
Article in PLoS computational biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
72 citing papers in PubMed.
- Clusters, fingers, and singles: A mechanical landscape of tumor invasion.PLoS computational biology · 2026Article
- The kinase ERK plays a conserved dominant role in the heterogeneity of epithelial-mesenchymal transition in pancreatic cancer cells.Science signaling · 2025Article
- Integrated mathematical and experimental modeling uncovers enhanced EMT plasticity upon loss of the DLC1 tumor suppressor.PLoS computational biology · 2025Article
- Exploring the role of EMT in ovarian cancer progression using a multiscale mathematical model.NPJ systems biology and applications · 2025Article
- A Boolean network model of hypoxia, mechanosensing and TGF-β signaling captures the role of phenotypic plasticity and mutations in tumor metastasis.PLoS computational biology · 2025Article
- Prolonged Low-Dose Administration of FDA-Approved Drugs for Non-Cancer Conditions: A Review of Potential Targets in Cancer Cells.International journal of molecular sciences · 2025Review
- An integrative phenotype-structured partial differential equation model for the population dynamics of epithelial-mesenchymal transition.NPJ systems biology and applications · 2025Article
- Fibrotic extracellular matrix preferentially induces a partial Epithelial-Mesenchymal Transition phenotype in a 3-D agent based model of fibrosis.Mathematical biosciences · 2025Article
- Phenotypic Plasticity, Non-genetic Mechanisms, and Immune Drug Resistance in Cancer.Cancer treatment and research · 2025Review
- Modelling variability and heterogeneity of EMT scenarios highlights nuclear positioning and protrusions as main drivers of extrusion.Nature communications · 2024Article
- Phenotypic Plasticity and Cancer: A System Biology Perspective.Journal of clinical medicine · 2024Review
- Spatial heterogeneity in tumor adhesion qualifies collective cell invasion.Biophysical journal · 2024Article
- Mesenchymal stem cells derived from CHIR99021 and TGF‑β induction remained on the colicomentum and improved cardiac function of a rat model of acute myocardium infarction.Experimental and therapeutic medicine · 2024Article
- A dynamic model of inorganic arsenic-induced carcinogenesis reveals an epigenetic mechanism for epithelial-mesenchymal plasticity.Environmental pollution (Barking, Essex : 1987) · 2024Article
- Cancer spreading patterns based on epithelial-mesenchymal plasticity.Frontiers in cell and developmental biology · 2024Article
- The epithelial-mesenchymal plasticity landscape: principles of design and mechanisms of regulation.Nature reviews. Genetics · 2023Review
- Population dynamics of EMT elucidates the timing and distribution of phenotypic intra-tumoral heterogeneity.iScience · 2023Article
- Multiscale Modeling of Spheroid Tumors: Effect of Nutrient Availability on Tumor Evolution.The journal of physical chemistry. B · 2023Article
- Boolean modeling of mechanosensitive epithelial to mesenchymal transition and its reversal.iScience · 2023Article
- Biophysical Parameters Can Induce Epithelial-to-Mesenchymal Phenotypic and Genotypic Changes in HT-29 Cells: A Preliminary Study.International journal of molecular sciences · 2023Article
12 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epithelial-mesenchymal heterogeneity implies that cells within the same tumor can exhibit different phenotypes-epithelial, mesenchymal, or one or more hybrid epithelial-mesenchymal phenotypes. This behavior has been reported across cancer types, both in vitro and in vivo, and implicated in multiple processes associated with metastatic aggressiveness including immune evasion, collective dissemination of tumor cells, and emergence of cancer cell subpopulations with stem cell-like properties. However, the ability of a population of cancer cells to generate, maintain, and propagate this heterogeneity has remained a mystifying feature. Here, we used a computational modeling approach to show that epithelial-mesenchymal heterogeneity can emerge from the noise in the partitioning of biomolecules (such as RNAs and proteins) among daughter cells during the division of a cancer cell. Our model captures the experimentally observed temporal changes in the fractions of different phenotypes in a population of murine prostate cancer cells, and describes the hysteresis in the population-level dynamics of epithelial-mesenchymal plasticity. The model is further able to predict how factors known to promote a hybrid epithelial-mesenchymal phenotype can alter the phenotypic composition of a population. Finally, we used the model to probe the implications of phenotypic heterogeneity and plasticity for different therapeutic regimens and found that co-targeting of epithelial and mesenchymal cells is likely to be the most effective strategy for restricting tumor growth. By connecting the dynamics of an intracellular circuit to the phenotypic composition of a population, our study serves as a first step towards understanding the generation and maintenance of non-genetic heterogeneity in a population of cancer cells, and towards the therapeutic targeting of phenotypic heterogeneity and plasticity in cancer cell populations.
Indexed as
Identifiers
What OpenQuestion holds
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.