Effects of Modifications in the Laminin-10 Basal Laminina on Prostate Cancer Invasion

Abstract

In order for prostate cancer to metastasize it must invade through a laminin-511 rich barrier. We have previously shown that the matrix metalloprotease MT1-MMP, which is expressed in prostate cancer but not in normal prostate tissue cleaves the laminin alpha-5 chain into four distinct fragments. This cleavage allows for increased prostate cancer cell migration in vitro. Laminin-511 cleavage also occurs in vivo in human prostate tissue. Cleavage of laminin-511 and release of laminin-511 fragments leads to altered cell function leading to increased cell migration and invasion in in vitro assays. We have demonstrated that prostate cancer cells treated with laminin-511 that has been cleaved by MT1-MMP have increased EGFR phosphorylation compared with cells grown on tissue culture plastic or intact laminin-511 in a Western blot. We have purified a recombinant 45kDa laminin-511 N-terminal cleavage fragment which contains laminin EGF-like domains. Treatment of prostate cancer cells with soluble recombinant fragment demonstrates that the cleaved laminin fragment acts as a matrikine, activating the EGFR on prostate cancer cells in a Western blot. This work demonstrates that increased MT1-MMP expression in prostate cancer not only cleaves the major laminin surrounding prostate cancer to clear a path for migration but also releases active fragments from the laminin-511 that signal for increased migration.

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Document Details

Document Type
Technical Report
Publication Date
Oct 01, 2006
Accession Number
ADA468686

Entities

People

  • Elisabeth L. Bair
  • Sangita C. Pawar

Organizations

  • University of Arizona

Tags

DTIC Thesaurus Topics

  • Anatomy
  • Biology
  • Cancer
  • Cell Biology
  • Cell Movement
  • Cells
  • Diseases And Disorders
  • Electronic Mail
  • Medical Personnel
  • Migration
  • Neoplasms
  • Oncology
  • Phosphorylation
  • Prostate Cancer
  • Tissue Culture
  • Tissues
  • Training

Fields of Study

  • Biology

Readers

  • Molecular Biology and Genetics
  • Oncology (Cancer Research).