ArticleOncotarget2020
Epigenetic feedback and stochastic partitioning during cell division can drive resistance to EMT.
Article in Oncotarget, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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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.
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Who cites it
23 citing papers in PubMed, 37 citations in OpenAlex.
- How cancer arises: Genetics releases, plasticity creates, genetics stabilizes.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- The regulatory network of epithelial-mesenchymal transition-associated non-coding RNAs in thyroid cancer: molecular mechanisms, clinical implications, and therapeutic strategies.Frontiers in oncology · 2025Review
- Dual role of GRHL3 in bladder carcinogenesis depending on histological subtypes.Molecular oncology · 2024Article
- The epithelial-mesenchymal plasticity landscape: principles of design and mechanisms of regulation.Nature reviews. Genetics · 2023Review
- Heterogeneity and plasticity of epithelial-mesenchymal transition (EMT) in cancer metastasis: Focusing on partial EMT and regulatory mechanisms.Cell proliferation · 2023Review
- Article
- Epigenetic factor competition reshapes the EMT landscape.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- P4HA2: A link between tumor-intrinsic hypoxia, partial EMT and collective migration.Advances in cancer biology - metastasis · 2022Article
- Revisiting the miR-200 Family: A Clan of Five Siblings with Essential Roles in Development and Disease.Biomolecules · 2022Review
- Emergent dynamics of a three-node regulatory network explain phenotypic switching and heterogeneity: a case study of Th1/Th2/Th17 cell differentiation.Molecular biology of the cell · 2022Article
- Interconnected high-dimensional landscapes of epithelial-mesenchymal plasticity and stemness in cancer.Clinical & experimental metastasis · 2022Review
- Population Dynamics of Epithelial-Mesenchymal Heterogeneity in Cancer Cells.Biomolecules · 2022Article
- Volumetric compression develops noise-driven single-cell heterogeneity.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Systems-level network modeling deciphers the master regulators of phenotypic plasticity and heterogeneity in melanoma.iScience · 2021Article
- KLF4 Induces Mesenchymal-Epithelial Transition (MET) by Suppressing Multiple EMT-Inducing Transcription Factors.Cancers · 2021Article
- Coupled Feedback Loops Involving PAGE4, EMT and Notch Signaling Can Give Rise to Non-genetic Heterogeneity in Prostate Cancer Cells.Entropy (Basel, Switzerland) · 2021Article
- NRF2-dependent Epigenetic Regulation can Promote the Hybrid Epithelial/Mesenchymal Phenotype.Frontiers in cell and developmental biology · 2021Article
- Epigenetic Regulation of Epithelial to Mesenchymal Transition in the Cancer Metastatic Cascade: Implications for Cancer Therapy.Frontiers in oncology · 2021Review
- Hybrid E/M Phenotype(s) and Stemness: A Mechanistic Connection Embedded in Network Topology.Journal of clinical medicine · 2020Article
- Hypoxia, partial EMT and collective migration: Emerging culprits in metastasis.Translational oncology · 2020Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epithelial-mesenchymal transition (EMT) and its reverse process mesenchymal-epithelial transition (MET) are central to metastatic aggressiveness and therapy resistance in solid tumors. While molecular determinants of both processes have been extensively characterized, the heterogeneity in the response of tumor cells to EMT and MET inducers has come into focus recently, and has been implicated in the failure of anti-cancer therapies. Recent experimental studies have shown that some cells can undergo an irreversible EMT depending on the duration of exposure to EMT-inducing signals. While the irreversibility of MET, or equivalently, resistance to EMT, has not been studied in as much detail, evidence supporting such behavior is slowly emerging. Here, we identify two possible mechanisms that can underlie resistance of cells to undergo EMT: epigenetic feedback in ZEB1/GRHL2 feedback loop and stochastic partitioning of biomolecules during cell division. Identifying the ZEB1/GRHL2 axis as a key determinant of epithelial-mesenchymal plasticity across many cancer types, we use mechanistic mathematical models to show how GRHL2 can be involved in both the abovementioned processes, thus driving an irreversible MET. Our study highlights how an isogenic population may contain subpopulation with varying degrees of susceptibility or resistance to EMT, and proposes a next set of questions for detailed experimental studies characterizing the irreversibility of MET/resistance to EMT.
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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.