ArticleNPJ systems biology and applications2015
Combinatorial interventions inhibit TGFβ-driven epithelial-to-mesenchymal transition and support hybrid cellular phenotypes.
Article in NPJ systems biology and applications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.
What it found
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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
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Who cites it
74 citing papers in PubMed, 150 citations in OpenAlex.
- Systems-level analysis identifies IRF6 as an inhibitor of epithelial-mesenchymal transition.Journal of biological engineering · 2026Article
- Succession-diagram-based Markov chains reveal the attractor landscape of asynchronous Boolean networks.NPJ systems biology and applications · 2026Article
- Circulating microRNAs in preterm white matter injury: a systems biology/qPCR-based pilot study.Pediatric research · 2026Article
- Automated model refinement using perturbation-observation pairs.NPJ systems biology and applications · 2025Article
- Systems Biology of the Cancer Cell.Annual review of biomedical engineering · 2025Review
- CanSeer: a translational methodology for developing personalized cancer models and therapeutics.Scientific reports · 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
- An integrative phenotype-structured partial differential equation model for the population dynamics of epithelial-mesenchymal transition.NPJ systems biology and applications · 2025Article
- Gene regulatory network inference during cell fate decisions by perturbation strategies.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
- Low dimensionality of phenotypic space as an emergent property of coordinated teams in biological regulatory networks.iScience · 2025Article
- AI-driven automated discovery tools reveal diverse behavioral competencies of biological networks.eLife · 2025Article
- A Boolean model explains phenotypic plasticity changes underlying hepatic cancer stem cells emergence.NPJ systems biology and applications · 2024Article
- Comprehensive molecular interaction map of TGFβ induced epithelial to mesenchymal transition in breast cancer.NPJ systems biology and applications · 2024Article
- Data- and theory-driven approaches for understanding paths of epithelial-mesenchymal transition.Genesis (New York, N.Y. : 2000) · 2024Review
- Proneural-mesenchymal antagonism dominates the patterns of phenotypic heterogeneity in glioblastoma.iScience · 2024Article
- Theoretical and computational tools to model multistable gene regulatory networks.Reports on progress in physics. Physical Society (Great Britain) · 2023Review
- Boolean modeling of mechanosensitive epithelial to mesenchymal transition and its reversal.iScience · 2023Article
- Dynamics of Epithelial-Mesenchymal Plasticity: What Have Single-Cell Investigations Elucidated So Far?ACS omega · 2023Review
- Quantifying cancer cell plasticity with gene regulatory networks and single-cell dynamics.Frontiers in network physiology · 2023Review
14 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Epithelial-to-mesenchymal transition (EMT) is a developmental process hijacked by cancer cells to leave the primary tumor site, invade surrounding tissue and establish distant metastases. A hallmark of EMT is the loss of E-cadherin expression, and one major signal for the induction of EMT is transforming growth factor beta (TGFβ), which is dysregulated in up to 40% of hepatocellular carcinoma (HCC). We aim to identify network perturbations that suppress TGFβ-driven EMT, with the goal of suppressing invasive properties of cancer cells. We use a systems-level Boolean dynamic model of EMT to systematically screen individual and combination perturbations (inhibition or constitutive activation of up to four nodes). We use a recently developed network control approach to understand the mechanism through which the combinatorial interventions suppress EMT. We test the results of our
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.