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Related Experiment Video

Updated: Oct 7, 2025

Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells
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CTCF Expression and Dynamic Motif Accessibility Modulates Epithelial-Mesenchymal Gene Expression.

Kelsey S Johnson1, Shaimaa Hussein2, Priyanka Chakraborty3

  • 1Department of Biology, Baylor University, Waco, TX 76706, USA.

Cancers
|January 11, 2022
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Summary

The chromatin insulator CTCF regulates epithelial-mesenchymal transition (EMT) plasticity. Its suppression maintains epithelial traits, while its upregulation promotes mesenchymal characteristics, impacting cancer metastasis.

Keywords:
ATAC-seqCTCFE-cadherinEMTMETchromatin accessibilitypartial EMT

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Area of Science:

  • Epigenetics and epigenomics
  • Cellular plasticity and cancer biology

Background:

  • Epithelial-mesenchymal transition (EMT) and its reversal (MET) are crucial for development and cancer progression, involving migration, invasion, and metastasis.
  • EMT is a reversible process regulated by epigenetic and epigenomic mechanisms.
  • Understanding the epigenomic regulation of EMT and its partial states is key to targeting cancer metastasis.

Purpose of the Study:

  • To investigate the epigenomic dynamics of reversible EMT and its partial states.
  • To elucidate the role of chromatin accessibility and specific proteins, like CTCF, in regulating EMT plasticity.

Main Methods:

  • Characterization of chromatin accessibility (ATAC-seq), transcriptomics, protein expression, and cellular phenotypes during stepwise reversible EMT.
  • Analysis of binding motifs, focusing on AP-1 family members and CTCF.
  • Loss-of-function experiments to assess the impact of CTCF suppression or upregulation on cellular plasticity and gene expression.

Main Results:

  • CTCF (chromatin insulator protein) is suppressed and re-expressed during EMT/MET, correlating with altered chromatin accessibility.
  • Early EMT phases show enrichment for AP-1 binding motifs and diminished CTCF binding motifs.
  • CTCF suppression enhances epithelial phenotype (upregulating E-cadherin/CDH1, downregulating N-cadherin/CDH2), while CTCF upregulation promotes mesenchymal traits.

Conclusions:

  • CTCF plays a significant role in regulating epithelial-mesenchymal plasticity.
  • CTCF levels directly influence the expression of EMT-related genes and cellular phenotypes.
  • Findings suggest CTCF as a potential target for modulating cancer cell plasticity and metastasis.