ArticleMolecular and cellular biology2016
Mesenchymal-Epithelial Transition in Sarcomas Is Controlled by the Combinatorial Expression of MicroRNA 200s and GRHL2.
Article in Molecular and cellular biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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Who cites it
57 citing papers in PubMed, 104 citations in OpenAlex.
- Sarcoma metastasis: distinct biological principles beyond the carcinoma paradigm.Cancer metastasis reviews · 2026Review
- Systems-level analysis identifies IRF6 as an inhibitor of epithelial-mesenchymal transition.Journal of biological engineering · 2026Article
- Extracellular vesicles modulate integrin signaling and subcellular energetics to promote pulmonary lymphangioleiomyomatosis metastasis.Communications biology · 2025Article
- A computational approach for perturbation-induced EMT transitions.NPJ systems biology and applications · 2025Article
- Microsatellite instability and PD-L1 expression in sarcomas: current evidence and clinical perspectives.Medical oncology (Northwood, London, England) · 2025Review
- GRHL2 regulates keratinocyte EMT-MET dynamics and scar formation during cutaneous wound healing.Cell death & disease · 2024Article
- Phenotypic Plasticity and Cancer: A System Biology Perspective.Journal of clinical medicine · 2024Review
- Dual role of CASP8AP2/FLASH in regulating epithelial-to-mesenchymal transition plasticity (EMP).Translational oncology · 2024Article
- Synthetic Epigenetic Reprogramming of Mesenchymal to Epithelial States Using the CRISPR/dCas9 Platform in Triple Negative Breast Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Dynamics of Epithelial-Mesenchymal Plasticity: What Have Single-Cell Investigations Elucidated So Far?ACS omega · 2023Review
- The ELF3 transcription factor is associated with an epithelial phenotype and represses epithelial-mesenchymal transition.Journal of biological engineering · 2023Article
- Epigenetic memory acquired during long-term EMT induction governs the recovery to the epithelial state.Journal of the Royal Society, Interface · 2023Article
- 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
- Article
- Transcriptional and post-transcriptional control of epithelial-mesenchymal plasticity: why so many regulators?Cellular and molecular life sciences : CMLS · 2022Review
- Reversion of methionine addiction of osteosarcoma cells to methionine independence results in loss of malignancy, modulation of the epithelial-mesenchymal phenotype and alteration of histone-H3 lysine-methylation.Frontiers in oncology · 2022Article
- Mapping phenotypic heterogeneity in melanoma onto the epithelial-hybrid-mesenchymal axis.Frontiers in oncology · 2022Article
- KLF4 Induces Mesenchymal-Epithelial Transition (MET) by Suppressing Multiple EMT-Inducing Transcription Factors.Cancers · 2021Article
- Lineage Plasticity in Cancer: The Tale of a Skin-Walker.Cancers · 2021Review
- Molecular mechanisms underpinning sarcomas and implications for current and future therapy.Signal transduction and targeted therapy · 2021Review
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
Abstract
Phenotypic plasticity involves a process in which cells transiently acquire phenotypic traits of another lineage. Two commonly studied types of phenotypic plasticity are epithelial-mesenchymal transition (EMT) and mesenchymal-epithelial transition (MET). In carcinomas, EMT drives invasion and metastatic dissemination, while MET is proposed to play a role in metastatic colonization. Phenotypic plasticity in sarcomas is not well studied; however, there is evidence that a subset of sarcomas undergo an MET-like phenomenon. While the exact mechanisms by which these transitions occur remain largely unknown, it is likely that some of the same master regulators that drive EMT and MET in carcinomas also act in sarcomas. In this study, we combined mathematical models with bench experiments to identify a core regulatory circuit that controls MET in sarcomas. This circuit comprises the microRNA 200 (miR-200) family, ZEB1, and GRHL2. Interestingly, combined expression of miR-200s and GRHL2 further upregulates epithelial genes to induce MET. This effect is phenocopied by downregulation of either ZEB1 or the ZEB1 cofactor, BRG1. In addition, an MET gene expression signature is prognostic for improved overall survival in sarcoma patients. Together, our results suggest that a miR-200, ZEB1, GRHL2 gene regulatory network may drive sarcoma cells to a more epithelial-like state and that this likely has prognostic relevance.
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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.