ArticleCancers2022
CTCF Expression and Dynamic Motif Accessibility Modulates Epithelial-Mesenchymal Gene Expression.
Article in Cancers, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
17 citing papers in PubMed, 25 citations in OpenAlex.
- Time-dependent memory of hypoxia exposure influences tumor invasion dynamics.bioRxiv : the preprint server for biology · 2026Article
- A Phenotype-Structured PDE Framework for Investigating the Role of Hypoxic Memory on Tumor Invasion under Cyclic Hypoxia.Bulletin of mathematical biology · 2026Article
- Targeting Tumour Heterogeneity through sequential timing of anti-hallmark combination therapies -a hypothesis for implementation.Frontiers in immunology · 2026Review
- Single-cell multiomic modelling of early metastatic events promoted by the extracellular matrix.British journal of cancer · 2025Article
- A phenotype-structured PDE framework for investigating the role of hypoxic memory on tumor invasion under cyclic hypoxia.bioRxiv : the preprint server for biology · 2025Article
- LncRNA MEG3/CTCF-CXCR4 axis functions in the regulation of breast cancer cell migration.Non-coding RNA research · 2025Article
- Article
- Regulating epithelial-mesenchymal plasticity from 3D genome organization.Communications biology · 2024Review
- Chromatin Organization and Transcriptional Programming of Breast Cancer Cell Identity.Endocrinology · 2023Review
- Dependency of NELF-E-SLUG-KAT2B epigenetic axis in breast cancer carcinogenesis.Nature communications · 2023Article
- Dynamics of Epithelial-Mesenchymal Plasticity: What Have Single-Cell Investigations Elucidated So Far?ACS omega · 2023Review
- CircSTK3 drives the metastasis of colorectal cancer by regulating epithelial-mesenchymal transition.iScience · 2023Article
- Article
- Epigenetic memory acquired during long-term EMT induction governs the recovery to the epithelial state.Journal of the Royal Society, Interface · 2023Article
- The Comparative Experimental Study of Sodium and Magnesium Dichloroacetate Effects on Pediatric PBT24 and SF8628 Cell Glioblastoma Tumors Using a Chicken Embryo Chorioallantoic Membrane Model and on Cells In Vitro.International journal of molecular sciences · 2022Article
- Regulation of epithelial-mesenchymal transition by protein lysine acetylation.Cell communication and signaling : CCS · 2022Review
- CTCF: A misguided jack-of-all-trades in cancer cells.Computational and structural biotechnology journal · 2022Review
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
Abstract
Epithelial-mesenchymal transition (EMT) and its reversal, mesenchymal-epithelial transition (MET) drive tissue reorganization critical for early development. In carcinomas, processing through EMT, MET, or partial states promotes migration, invasion, dormancy, and metastatic colonization. As a reversible process, EMT is inherently regulated at epigenetic and epigenomic levels. To understand the epigenomic nature of reversible EMT and its partial states, we characterized chromatin accessibility dynamics, transcriptomic output, protein expression, and cellular phenotypes during stepwise reversible EMT. We find that the chromatin insulating protein machinery, including CTCF, is suppressed and re-expressed, coincident with broad alterations in chromatin accessibility, during EMT/MET, and is lower in triple-negative breast cancer cell lines with EMT features. Through an analysis of chromatin accessibility using ATAC-seq, we identify that early phases of EMT are characterized by enrichment for AP-1 family member binding motifs, but also by a diminished enrichment for CTCF binding motifs. Through a loss-of-function analysis, we demonstrate that the suppression of CTCF alters cellular plasticity, strengthening the epithelial phenotype via the upregulation of epithelial markers E-cadherin/CDH1 and downregulation of N-cadherin/CDH2. Conversely, the upregulation of CTCF leads to the upregulation of EMT gene expression and an increase in mesenchymal traits. These findings are indicative of a role of CTCF in regulating epithelial-mesenchymal plasticity and gene expression.
Indexed as
Identifiers
What OpenQuestion holds
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.