ArticleCancer research2023
A Cell-Fate Reprogramming Strategy Reverses Epithelial-to-Mesenchymal Transition of Lung Cancer Cells While Avoiding Hybrid States.
Article in Cancer research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 20 citations in OpenAlex.
- Systems-level analysis identifies IRF6 as an inhibitor of epithelial-mesenchymal transition.Journal of biological engineering · 2026Article
- Mesenchymal to epithelial transition (MET) in cancer progression: insights from logical modeling.Scientific reports · 2026Article
- Emerging research themes in drug resistance in osteosarcoma: a 25-year bibliometric and visualized analysis.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Oncogenic H-Ras Reprograms Madin-Darby Canine Kidney (MDCK) Cell-Derived Midbody Remnant Proteome Following Epithelial-Mesenchymal Transition.Proteomics · 2026Article
- Reverse control of biological networks to restore phenotype landscapes.Science advances · 2025Article
- Transition paths across the epithelial-mesenchymal transition landscape are dictated by network logic.Development (Cambridge, England) · 2025Article
- Article
- Attractor Landscape Analysis Reveals a Reversion Switch in the Transition of Colorectal Tumorigenesis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Advances in modeling cellular state dynamics: integrating omics data and predictive techniques.Animal cells and systems · 2025Review
- Canalizing kernel for cell fate determination.Briefings in bioinformatics · 2024Article
- Decoding the principle of cell-fate determination for its reverse control.NPJ systems biology and applications · 2024Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The epithelial-to-mesenchymal transition (EMT) of primary cancer contributes to the acquisition of lethal properties, including metastasis and drug resistance. Blocking or reversing EMT could be an effective strategy to improve cancer treatment. However, it is still unclear how to achieve complete EMT reversal (rEMT), as cancer cells often transition to hybrid EMT states with high metastatic potential. To tackle this problem, we employed a systems biology approach and identified a core-regulatory circuit that plays the primary role in driving rEMT without hybrid properties. Perturbation of any single node was not sufficient to completely revert EMT. Inhibition of both SMAD4 and ERK signaling along with p53 activation could induce rEMT in cancer cells even with TGFβ stimulation, a primary inducer of EMT. Induction of rEMT in lung cancer cells with the triple combination approach restored chemosensitivity. This cell-fate reprogramming strategy based on attractor landscapes revealed potential therapeutic targets that can eradicate metastatic potential by subverting EMT while avoiding hybrid states. SIGNIFICANCE: Network modeling unravels the highly complex and plastic process regulating epithelial and mesenchymal states in cancer cells and discovers therapeutic interventions for reversing epithelial-to-mesenchymal transition and enhancing chemosensitivity.
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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.