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Loss of E-cadherin promotes metastasis via multiple downstream transcriptional pathways

Tamer T Onder1, Piyush B Gupta, Sendurai A Mani

  • 1Whitehead Institute for Biomedical Research, Cambridge, Massachusetts, USA.

Cancer Research
|May 17, 2008
PubMed

Insights

Loss of E-cadherin protein, not just cell-cell contact disruption, drives metastasis. This involves epithelial-to-mesenchymal transition and requires transcription factors like Twist for tumor spread.

Area of Science:

  • Molecular biology
  • Cancer research
  • Cell biology

Background:

  • E-cadherin loss is linked to metastasis by disrupting cell adhesion.
  • Understanding the molecular mechanisms is crucial for cancer treatment.

Purpose of the Study:

  • To differentiate the roles of E-cadherin's adhesion and signaling functions in metastasis.
  • To elucidate the molecular pathways initiated by E-cadherin loss.

Main Methods:

  • Inhibition of E-cadherin function using two distinct methods.
  • Analysis of epithelial-to-mesenchymal transition, invasiveness, and anoikis resistance.
  • Gene expression profiling and identification of key transcription factors.

Main Results:

  • Disrupting cell-cell contacts alone did not induce metastasis.
  • Loss of E-cadherin protein triggered epithelial-to-mesenchymal transition, invasiveness, and anoikis resistance.
  • Beta-catenin was necessary but not sufficient; Twist transcription factor was essential for metastasis.

Conclusions:

  • E-cadherin loss is a critical driver of tumor metastasis.
  • Metastasis involves significant transcriptional and functional changes induced by E-cadherin loss.
  • Targeting E-cadherin-induced pathways, like Twist, may offer therapeutic strategies.

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