Adhesive Mechanisms in Breast Cancer Metastasis

Abstract

Complications from metastatic disease are the primary cause of death in breast cancer. We found that human breast cancer cells can express the adhesion receptor integrin alpha v beta 3 in an activated or a non-activated functional form. Expression of the activated, but not the non-activated receptor supports metastatic dissemination. Mechanisms through which activated integrin alpha v beta 3 promotes metastasis include: binding of soluble ligand, support of tumor cell arrest during blood flow through tumor cell interaction with platelets, and promotion of breast cancer cell migration. Activated integrin alpha v beta 3 promotes breast cancer migration by cooperating with metalloproteinase MMP-9. A model mechanism for this cooperation is proposed. Our new findings support the originally proposed concept, that activation of breast cancer cell integrin alpha v beta 3 supports the metastatic phenotype in the tumor cells. Thus, these studies identify activated alpha v beta 3 as a new functional marker of metastatic breast cancer cells and indicate that activated alpha v beta 3 should be considered as a novel target for the inhibition of breast cancer metastasis.

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Document Details

Document Type
Technical Report
Publication Date
Oct 01, 2001
Accession Number
ADA403354

Entities

People

  • Brunhilde Felding-habermann

Organizations

  • Scripps Research

Tags

DTIC Thesaurus Topics

  • Adhesion
  • Adhesives
  • Blood
  • Blood Cells
  • Blood Flow
  • Breast Cancer
  • Cancer
  • Cell Line
  • Cell Movement
  • Cell Physiological Processes
  • Cells
  • Diseases And Disorders
  • Endothelial Cells
  • Genes
  • Metastasis
  • Neoplasms
  • Oncology

Fields of Study

  • Biology

Readers

  • Analytical Mechanics
  • Breast cancer cell signaling and growth regulation.
  • Molecular Biology and Genetics