ArticleGenome biology2013
Architecture of epigenetic reprogramming following Twist1-mediated epithelial-mesenchymal transition.
Article in Genome biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 1 of them a synthesis that pooled it.
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Who cites it
52 citing papers in PubMed, 1 synthesis or guideline pooled it.
- The lactate-lactylation axis in renal fibrosis: potential mechanisms in diabetic kidney disease.Annals of medicine · 2025Pooled it
- Opposite patterns of association of TWIST1 expression with patient survival in SHH and Group 4 medulloblastoma.Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2025Article
- Targeted disruption of PRC1.1 complex enhances bone remodeling.Nature communications · 2025Article
- EZH2 promotes malignant biological behavior in esophageal squamous cell carcinoma via EMT.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2025Article
- Exploration of the biological mechanisms of CENPA as an oncogene in glioma: Screening based on cancer functional status.Journal of cellular and molecular medicine · 2024Article
- Factors Determining Epithelial-Mesenchymal Transition in Cancer Progression.International journal of molecular sciences · 2024Review
- Regulating epithelial-mesenchymal plasticity from 3D genome organization.Communications biology · 2024Review
- Zeb1-controlled metabolic plasticity enables remodeling of chromatin accessibility in the development of neuroendocrine prostate cancer.Cell death and differentiation · 2024Article
- Epithelial-to-mesenchymal plasticity from development to disease: An introduction to the special issue.Genesis (New York, N.Y. : 2000) · 2024Article
- Epithelial specific splicing regulator proteins as emerging oncogenes in aggressive prostate cancer.Oncogene · 2023Review
- LRRC15 expression indicates high level of stemness regulated by TWIST1 in mesenchymal stem cells.iScience · 2023Article
- EMT/MET plasticity in cancer and Go-or-Grow decisions in quiescence: the two sides of the same coin?Molecular cancer · 2023Review
- Modulating epigenetic modifications for cancer therapy (Review).Oncology reports · 2023Review
- CTCF Expression and Dynamic Motif Accessibility Modulates Epithelial-Mesenchymal Gene Expression.Cancers · 2022Article
- Connections between metabolism and epigenetic modifications in cancer.Medical review (2021) · 2021Review
- Epithelial-mesenchymal transition sensitizes breast cancer cells to cell death via the fungus-derived sesterterpenoid ophiobolin A.Scientific reports · 2021Article
- Symmetry breaking of tissue mechanics in wound induced hair follicle regeneration of laboratory and spiny mice.Nature communications · 2021Article
- Article
- Prominent Role of Histone Modifications in the Regulation of Tumor Metastasis.International journal of molecular sciences · 2021Review
- Interactions and Feedbacks in E-Cadherin Transcriptional Regulation.Frontiers in cell and developmental biology · 2021Article
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Authors and funding
17 authors.
Funding
Abstract
backgroundEpithelial-mesenchymal transition (EMT) is known to impart metastasis and stemness characteristics in breast cancer. To characterize the epigenetic reprogramming following Twist1-induced EMT, we characterized the epigenetic and transcriptome landscapes using whole-genome transcriptome analysis by RNA-seq, DNA methylation by digital restriction enzyme analysis of methylation (DREAM) and histone modifications by CHIP-seq of H3K4me3 and H3K27me3 in immortalized human mammary epithelial cells relative to cells induced to undergo EMT by Twist1.
resultsEMT is accompanied by focal hypermethylation and widespread global DNA hypomethylation, predominantly within transcriptionally repressed gene bodies. At the chromatin level, the number of gene promoters marked by H3K4me3 increases by more than one fifth; H3K27me3 undergoes dynamic genomic redistribution characterized by loss at half of gene promoters and overall reduction of peak size by almost half. This is paralleled by increased phosphorylation of EZH2 at serine 21. Among genes with highly altered mRNA expression, 23.1% switch between H3K4me3 and H3K27me3 marks, and those point to the master EMT targets and regulators CDH1, PDGFRα and ESRP1. Strikingly, Twist1 increases the number of bivalent genes by more than two fold. Inhibition of the H3K27 methyltransferases EZH2 and EZH1, which form part of the Polycomb repressive complex 2 (PRC2), blocks EMT and stemness properties.
conclusionsOur findings demonstrate that the EMT program requires epigenetic remodeling by the Polycomb and Trithorax complexes leading to increased cellular plasticity. This suggests that inhibiting epigenetic remodeling and thus decrease plasticity will prevent EMT, and the associated breast cancer metastasis.
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