ArticleScientific reports2015
Modeling the Transitions between Collective and Solitary Migration Phenotypes in Cancer Metastasis.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed.
- Review
- Mechanical observables of cancer invasion: actin, adhesion, and metastatic plasticity.Frontiers in cell and developmental biology · 2026Review
- Gene regulatory network inference during cell fate decisions by perturbation strategies.NPJ systems biology and applications · 2025Article
- The metastatic cascade through the lens of therapeutic inhibition.Cell reports. Medicine · 2025Review
- General relationship of local topologies, global dynamics, and bifurcation in cellular networks.NPJ systems biology and applications · 2024Article
- A Recipe for Successful Metastasis: Transition and Migratory Modes of Ovarian Cancer Cells.Cancers · 2024Review
- Origin, heterogeneity, and interconversion of noncanonical bistable switches from the positive feedback loops under dual signaling.iScience · 2023Article
- Epithelial plasticity in COPD results in cellular unjamming due to an increase in polymerized actin.Journal of cell science · 2022Article
- Review
- Modeling extracellular matrix through histo-molecular gradient in NSCLC for clinical decisions.Frontiers in oncology · 2022Article
- Density-Dependent Migration Characteristics of Cancer Cells Driven by Pseudopod Interaction.Frontiers in cell and developmental biology · 2022Article
- A requirement for p120-catenin in the metastasis of invasive ductal breast cancer.Journal of cell science · 2021Article
- Multi-Stability and Consequent Phenotypic Plasticity in AMPK-Akt Double Negative Feedback Loop in Cancer Cells.Journal of clinical medicine · 2021Article
- Machine learning and deep learning methods that use omics data for metastasis prediction.Computational and structural biotechnology journal · 2021Review
- Identifying inhibitors of epithelial-mesenchymal plasticity using a network topology-based approach.NPJ systems biology and applications · 2020Article
- Emergent Properties of the HNF4α-PPARγ Network May Drive Consequent Phenotypic Plasticity in NAFLD.Journal of clinical medicine · 2020Article
- Comparative Study of Transcriptomics-Based Scoring Metrics for the Epithelial-Hybrid-Mesenchymal Spectrum.Frontiers in bioengineering and biotechnology · 2020Article
- Boolean model of anchorage dependence and contact inhibition points to coordinated inhibition but semi-independent induction of proliferation and migration.Computational and structural biotechnology journal · 2020Article
- Actin cytoskeleton in mesenchymal-to-amoeboid transition of cancer cells.International review of cell and molecular biology · 2020Review
- Review
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cellular plasticity during cancer metastasis is a major clinical challenge. Two key cellular plasticity mechanisms -Epithelial-to-Mesenchymal Transition (EMT) and Mesenchymal-to-Amoeboid Transition (MAT) - have been carefully investigated individually, yet a comprehensive understanding of their interconnections remains elusive. Previously, we have modeled the dynamics of the core regulatory circuits for both EMT (miR-200/ZEB/miR-34/SNAIL) and MAT (Rac1/RhoA). We now extend our previous work to study the coupling between these two core circuits by considering the two microRNAs (miR-200 and miR-34) as external signals to the core MAT circuit. We show that this coupled circuit enables four different stable steady states (phenotypes) that correspond to hybrid epithelial/mesenchymal (E/M), mesenchymal (M), amoeboid (A) and hybrid amoeboid/mesenchymal (A/M) phenotypes. Our model recapitulates the metastasis-suppressing role of the microRNAs even in the presence of EMT-inducing signals like Hepatocyte Growth Factor (HGF). It also enables mapping the microRNA levels to the transitions among various cell migration phenotypes. Finally, it offers a mechanistic understanding for the observed phenotypic transitions among different cell migration phenotypes, specifically the Collective-to-Amoeboid Transition (CAT).
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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.