Vitamin A Regulation of Cadherins in Breast Cancer

Abstract

Vitamin a derivatives (retinoids) are known to be potent regulators of cell proliferation and epithelial cell differentiation and specifically inhibit the growth of several cancers. The mechanisms of action of retinoids are just starting to be understood. For example, retinoids are known to inhibit the junction of AP-1, a transcription factor complex that is involved in cell proliferation and neoplastic transformation. Retinoids are also known to stabilize components of the adherens junction, the junction of which is essential in preventing tumor progression and invasion. Previously, we have shown that in a breast cancer cell line, 9-cis retinoic acid induces a dramatic change in cell morphology, an increase in cell-cell adhesion strength, a decrease in cell proliferation, and an increase in the expression of the adherens junction molecule, beta-catenin. This work now demonstrates that retinoic acid also induces the expression of a cadherin and that the expression of a cadherin, not of beta-catenin is necessary and sufficient to mimic the effects induced by retinoic acid. Furthermore, this work also gives strong evidence to suggest that retinoic acid inhibits the beta-catenin mediated cell signaling pathway, although in a manner independent of cadherin function.

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Document Details

Document Type
Technical Report
Publication Date
May 01, 2000
Accession Number
ADA389346

Entities

People

  • Michael Pishvaian
  • Stephen Byers

Organizations

  • Georgetown University

Tags

DTIC Thesaurus Topics

  • Antineoplastic Agents
  • Biomedical Research
  • Breast Cancer
  • Cell Line
  • Cell Membrane
  • Cell Physiological Processes
  • Cells
  • Chemistry
  • Cytoskeleton
  • Epithelial Cells
  • Intercellular Junctions
  • Lymphocytes
  • Materials
  • Molecules
  • Neoplasms
  • Peptide Growth Factors
  • Proteins

Fields of Study

  • Biology

Readers

  • Molecular Biology and Genetics