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Updated: Jun 14, 2026

Induction and Analysis of Epithelial to Mesenchymal Transition
10:37

Induction and Analysis of Epithelial to Mesenchymal Transition

Published on: August 27, 2013

Kruppel-like factor 4 inhibits epithelial-to-mesenchymal transition through regulation of E-cadherin gene expression

Jennifer L Yori1, Emhonta Johnson, Guangjin Zhou

  • 1Department of Pharmacology, Case Western Reserve University, Cleveland, Ohio 44106, USA.

The Journal of Biological Chemistry
|April 2, 2010
PubMed

Insights

Krüppel-like factor 4 (KLF4) maintains epithelial characteristics in breast cells by regulating E-cadherin. This finding suggests KLF4 acts as a tumor suppressor, inhibiting metastasis in breast cancer.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Cancer Research

Background:

  • Krüppel-like factor 4 (KLF4) is a transcriptional regulator involved in cell proliferation and differentiation.
  • While KLF4 acts as a tumor suppressor in some tissues, its role in breast cancer remains unclear.

Purpose of the Study:

  • To investigate the function of KLF4 in maintaining the epithelial phenotype in mammary epithelial cells.
  • To determine if KLF4 regulates E-cadherin expression and influences epithelial-to-mesenchymal transition (EMT) in breast cancer.

Main Methods:

  • KLF4 silencing in MCF-10A mammary epithelial cells.
  • Analysis of epithelial cell morphology, migration, and E-cadherin expression (protein and mRNA).
  • Promoter/reporter assays and chromatin immunoprecipitation to assess KLF4 binding to the E-cadherin promoter.
  • Forced KLF4 expression in MDA-MB-231 breast cancer cells to evaluate effects on migration and invasion.

Main Results:

  • KLF4 is essential for maintaining the epithelial phenotype in non-transformed mammary cells.
  • KLF4 silencing induced changes in cell morphology and migration, characteristic of EMT, and decreased E-cadherin levels.
  • KLF4 directly binds to and activates the E-cadherin promoter.
  • Restoring KLF4 expression in metastatic breast cancer cells suppressed migration and invasion.

Conclusions:

  • E-cadherin is identified as a novel transcriptional target of KLF4.
  • KLF4 plays a critical role in maintaining E-cadherin expression and preventing EMT in mammary epithelial cells.
  • These findings support a metastasis-suppressive role for KLF4 in breast cancer.

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