ArticleJournal of the Royal Society, Interface2020
Systems biology approach suggests new miRNAs as phenotypic stability factors in the epithelial-mesenchymal transition.
Article in Journal of the Royal Society, Interface, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed.
- Review
- Network hypermotifs in biological systems: structure, dynamics, and functional implications.NPJ systems biology and applications · 2026Review
- PseudoCell: A Multivalued Logical Regulatory Network to Investigate Premature Senescence Dynamics and Heterogeneity.Aging medicine (Milton (N.S.W)) · 2025Article
- An integrative phenotype-structured partial differential equation model for the population dynamics of epithelial-mesenchymal transition.NPJ systems biology and applications · 2025Article
- Review
- Operating principles of interconnected feedback loops driving cell fate transitions.NPJ systems biology and applications · 2025Article
- Proneural-mesenchymal antagonism dominates the patterns of phenotypic heterogeneity in glioblastoma.iScience · 2024Article
- A dynamic Boolean network reveals that the BMI1 and MALAT1 axis is associated with drug resistance by limiting miR-145-5p in non-small cell lung cancer.Non-coding RNA research · 2024Article
- The lncRNA DLX6-AS1/miR-16-5p axis regulates autophagy and apoptosis in non-small cell lung cancer: A Boolean model of cell death.Non-coding RNA research · 2023Article
- A model for the dissemination of circulating tumour cell clusters involving platelet recruitment and a plastic switch between cooperative and individual behaviours.BMC ecology and evolution · 2023Article
- Article
- Network motifs and hypermotifs in TGFβ-induced epithelial to mesenchymal transition and metastasis.Frontiers in systems biology · 2023Article
- Network topology metrics explaining enrichment of hybrid epithelial/mesenchymal phenotypes in metastasis.PLoS computational biology · 2022Article
- Network analysis reveals that the tumor suppressor lncRNA GAS5 acts as a double-edged sword in response to DNA damage in gastric cancer.Scientific reports · 2022Article
- Article
- Interconnected high-dimensional landscapes of epithelial-mesenchymal plasticity and stemness in cancer.Clinical & experimental metastasis · 2022Review
- Dynamical modeling of miR-34a, miR-449a, and miR-16 reveals numerous DDR signaling pathways regulating senescence, autophagy, and apoptosis in HeLa cells.Scientific reports · 2022Article
- A Boolean Model of the Proliferative Role of the lncRNA XIST in Non-Small Cell Lung Cancer Cells.Biology · 2022Article
- Transcriptional and post-transcriptional control of epithelial-mesenchymal plasticity: why so many regulators?Cellular and molecular life sciences : CMLS · 2022Review
- Dynamical Analysis of a Boolean Network Model of the Oncogene Role of lncRNA ANRIL and lncRNA UFC1 in Non-Small Cell Lung Cancer.Biomolecules · 2022Article
Corrections and comments
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3 authors.
Funding
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Abstract
The epithelial-mesenchymal transition (EMT) is a cellular programme on which epithelial cells undergo a phenotypic transition to mesenchymal ones acquiring metastatic properties such as mobility and invasion. TGF-β signalling can promote the EMT process. However, the dynamics of the concentration response of TGF-β-induced EMT is not well explained. In this work, we propose a logical model of TGF-β dose dependence of EMT in MCF10A breast cells. The model outcomes agree with experimentally observed phenotypes for the wild-type and perturbed/mutated cases. As important findings of the model, it predicts the coexistence of more than one hybrid state and that the circuit between TWIST1 and miR-129 is involved in their stabilization. Thus, miR-129 should be considered as a phenotypic stability factor. The circuit TWIST1/miR-129 associates with ZEB1-mediated circuits involving miRNAs 200, 1199, 340, and the protein GRHL2 to stabilize the hybrid state. Additionally, we found a possible new autocrine mechanism composed of the circuit involving TGF-β, miR-200, and SNAIL1 that contributes to the stabilization of the mesenchymal state. Therefore, our work can extend our comprehension of TGF-β-induced EMT in MCF10A cells to potentially improve the strategies for breast cancer treatment.
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