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Related Experiment Videos

Tumour-associated E-cadherin mutations alter cellular morphology, decrease cellular adhesion and increase cellular

G Handschuh1, S Candidus, B Luber

  • 1GSF-Forschungszentrum für Umwelt and Gesundheit, Institut für Pathologie, Neuherberg, Germany.

Oncogene
|August 10, 1999
PubMed
Summary
This summary is machine-generated.

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Tumor-associated mutations in E-cadherin, a cell adhesion molecule, disrupt cell shape and increase motility. These E-cadherin gene mutations may drive invasive behaviors in gastric cancers.

Area of Science:

  • Cell Biology
  • Molecular Oncology
  • Biochemistry

Background:

  • E-cadherin is crucial for cell adhesion and tissue integrity.
  • E-cadherin deficiency in tumors correlates with altered cell morphology, motility, and invasion.
  • Tumorigenic mutations can affect the extracellular domain of E-cadherin, impacting its function.

Purpose of the Study:

  • To investigate the functional consequences of specific E-cadherin mutations found in gastric carcinomas.
  • To analyze how mutations in exons 8 and 9 of E-cadherin affect cell morphology, adhesion, motility, and cytoskeleton organization.
  • To determine if these mutations act in a trans-dominant-active manner to promote cell invasion.

Main Methods:

  • Stable transfection of human breast carcinoma cells (MDA-MB-435S) and mouse fibroblasts (L cells) with wild-type and mutant E-cadherin cDNAs.

Related Experiment Videos

  • Analysis of E-cadherin localization, cell morphology, calcium-dependent cell aggregation, cell motility, and actin cytoskeleton organization.
  • Comparison of cellular behaviors between cells expressing wild-type and mutant E-cadherin.

    • Main Results:

    • Mutant E-cadherin expression resulted in irregular cell shapes and scattered appearance, particularly with exon 8 mutations.
    • Mutant E-cadherins showed altered localization, including apical and perinuclear patterns, with reduced actin filaments.
    • Cells expressing mutant E-cadherin exhibited decreased cell aggregation and significantly increased cell motility.
    • Exon 8 mutations led to the most pronounced scattered morphology and motility changes.

    Conclusions:

    • E-cadherin mutations in exons 8 or 9 disrupt cell adhesion and induce significant changes in cell morphology and motility.
    • These mutations appear to act in a trans-dominant-active manner, promoting increased cell motility and potentially invasive behavior.
    • The findings suggest a causal link between E-cadherin mutations in exons 8/9 and the invasive phenotype observed in diffuse-type gastric carcinomas.