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Related Experiment Videos

Cadherin switch in tumor progression.

Rachel B Hazan1, Rui Qiao, Rinat Keren

  • 1Department of Pathology, Albert Einstein College of Medicine, Bronx, New York 10461, USA. rhazan@aecom.yu.edu

Annals of the New York Academy of Sciences
|May 22, 2004
PubMed
Summary

The switch from E-cadherin to N-cadherin promotes cancer invasion and metastasis in epithelial carcinomas. This change in cell adhesion molecules facilitates tumor cell spread and the acquisition of an invasive phenotype.

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Area of Science:

  • Oncology
  • Cell Biology
  • Molecular Biology

Background:

  • E-cadherin loss is a known driver of epithelial carcinoma invasion.
  • N-cadherin upregulation is observed in invasive tumor cells, correlating with dedifferentiation.

Purpose of the Study:

  • To summarize the E-cadherin to N-cadherin switch in epithelial carcinomas.
  • To explore the impact of this switch on metastatic progression.

Main Methods:

  • Review of recent evidence on cadherin expression in cancer.
  • Analysis of N-cadherin's role in tumor cell motility, invasion, and metastasis.
  • Examination of N-cadherin's signaling interactions (e.g., with FGF receptor).

Main Results:

Related Experiment Videos

  • N-cadherin expression correlates with increased tumor cell motility, invasion, and metastasis.
  • N-cadherin signaling up-modulates MMP-9, enhancing cellular invasion.
  • N-cadherin may aid tumor cell dissemination by promoting interactions with stroma and endothelium.

    • Conclusions:

    • The E-cadherin to N-cadherin switch is a critical event in epithelial carcinoma progression.
    • N-cadherin plays a multifaceted role in promoting cancer metastasis.
    • Targeting N-cadherin may offer therapeutic strategies against cancer spread.