Met (HGF Receptor) in Breast Cancer

Abstract

The hepatocyte growth factor (HGF)/Met signaling pathway has been shown to be important for stimulating cell proliferation, motility, invasion and metastasis. Recent work from our lab has identified a 60 kDa fragment from the carboxy-terminal domain of Met that localizes to the nucleus. Preliminary data from our also indicates that Met is translocated to the nucleus during in vitro wound healing of epithelial sheets of cells, but appears to be antibody dependent as a newly validated mouse monoclonal antibody does not detect the 60 kDa fragment. Because several pharmaceutical companies are currently developing Met-based therapies, it becomes even more important to gain an understanding of the role of nuclear Met, especially whether or not it may be contributing to invasion and metastasis. To date, no studies have been conducted to understand this aspect of Met function. Therefore the objectives of my proposal are to assess the role of Met in a model of epithelial-mesenchymal transition (EMT), identify key residues in the Met receptor necessary for nuclear translocation, and determine the functional role of Met in the nucleus.

Open PDF

Document Details

Document Type
Technical Report
Publication Date
Sep 01, 2010
Accession Number
ADA535659

Entities

People

  • Jennifer Bordeaux

Organizations

  • Yale University

Tags

DTIC Thesaurus Topics

  • Antibodies
  • Biomedical Research
  • Breast Cancer
  • Cancer
  • Cell Line
  • Cells
  • Demographic Cohorts
  • Epithelial Cells
  • Growth Factors
  • Inhibition
  • Metastasis
  • Molecules
  • Neoplasms
  • Proteins
  • Terminals
  • Transitions
  • Wound Healing

Fields of Study

  • Biology

Readers

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