Related Experiment Video

Updated: Jul 9, 2026

Detection of Alternative Splicing During Epithelial-Mesenchymal Transition
11:48

Detection of Alternative Splicing During Epithelial-Mesenchymal Transition

Published on: October 9, 2014

Twist is a transcriptional repressor of E-cadherin gene expression in breast cancer

Farhad Vesuna1, Paul van Diest, Ji Hshiung Chen

  • 1Department of Radiology, Johns Hopkins University School of Medicine, 340 Traylor , 720 Rutland Avenue, Baltimore, MD 21205, USA.

Biochemical and Biophysical Research Communications
|December 8, 2007
PubMed

Insights

Twist, a key protein in development and cancer, was found to repress E-cadherin gene expression in breast cancer cells. This study confirms Twist’s role in down-regulating E-cadherin, impacting breast cancer progression.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Genetics

Background:

  • Twist is a basic helix-loop-helix protein implicated in human development and cancer.
  • Twist influences breast epithelial cell transformation.
  • E-cadherin is a crucial cell adhesion molecule often downregulated in cancer.

Purpose of the Study:

  • To investigate the role of Twist in regulating E-cadherin expression in breast cancer.
  • To determine if Twist transcriptionally represses E-cadherin.
  • To validate the functional relevance of Twist-mediated E-cadherin regulation in clinical samples.

Main Methods:

  • Transient promoter assays to assess E-cadherin promoter activity.
  • Immunoblot analyses to evaluate E-cadherin protein levels upon Twist overexpression.
  • Chromatin immunoprecipitation (ChIP) to confirm Twist binding to the E-cadherin promoter.
  • Quantitative real-time PCR and immunohistochemistry on patient samples.

Main Results:

  • Twist significantly down-regulates E-cadherin promoter activity by up to two-fold.
  • Overexpression of Twist leads to decreased E-cadherin protein levels in breast cancer cell lines.
  • Chromatin immunoprecipitation confirmed direct binding of Twist to the E-cadherin promoter.
  • Functional relevance was validated in a cohort of breast cancer samples.

Conclusions:

  • Twist transcriptionally represses E-cadherin in breast cancer cells.
  • This regulation by Twist contributes to alterations in E-cadherin levels during breast cancer progression.
  • The findings highlight a novel mechanism involving Twist in breast cancer pathogenesis.

More Related Videos

Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells06:54

Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells

Published on: October 27, 2020

Related Concept Videos

Cadherins in Tissue Organization01:19

Cadherins in Tissue Organization

The cadherins are a superfamily of cell adhesion molecules comprising over 180 variants, with specific tissues expressing a particular combination of cadherin types. Cadherins generally exhibit homophilic binding; i.e., cadherins on one cell bind to cadherins of the same or closely related type on another cell. Thus, cells of the same type have a specific affinity to bind to each other and sort themselves into clusters to form tissues.
Cell Sorting During Development
Cell sorting plays an...
Canonical Wnt Signaling Pathway02:54

Canonical Wnt Signaling Pathway

The gene encoding the main signaling molecules of the Wnt signaling pathways (the Wnt proteins) was discovered almost four decades ago by Nüsslein-Volhard and Wieschaus. They identified and originally named the gene "wingless" (wg) after a phenotype discovered during their landmark genetic screen in Drosophila for body pattern defects. At around the same time, another researcher named Harold Varmus found that a murine tumor virus activates the mammalian wg homolog, Int-1, which results in tumor...
Canonical Wnt Signaling Pathway02:54

Canonical Wnt Signaling Pathway

The gene encoding the main signaling molecules of the Wnt signaling pathways (the Wnt proteins) was discovered almost four decades ago by Nüsslein-Volhard and Wieschaus. They identified and originally named the gene "wingless" (wg) after a phenotype discovered during their landmark genetic screen in Drosophila for body pattern defects. At around the same time, another researcher named Harold Varmus found that a murine tumor virus activates the mammalian wg homolog, Int-1, which results in tumor...
Master Transcription Regulators02:23

Master Transcription Regulators

Master transcription regulators are regulatory proteins that are predominantly responsible for regulating the expression of multiple genes. Often these genes work in concert to drive a  complex process. Activation of a master transcription regulator can lead to a cascade of transcriptional activation necessary for that outcome. These regulators can directly bind to the regulatory sequences of the various genes involved, or they can indirectly regulate transcription by binding to regulatory...
Master Transcription Regulators02:23

Master Transcription Regulators

Master transcription regulators are regulatory proteins that are predominantly responsible for regulating the expression of multiple genes. Often these genes work in concert to drive a  complex process. Activation of a master transcription regulator can lead to a cascade of transcriptional activation necessary for that outcome. These regulators can directly bind to the regulatory sequences of the various genes involved, or they can indirectly regulate transcription by binding to regulatory...
Metastasis02:30

Metastasis

Metastasis is the spread of cancer cells from the original site to distant locations in the body. Cancer cells can spread via blood vessels (hematogenous) as well as lymph vessels in the body.
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...