Studying the Roles of GRK2-Mediated Smad2/3 Phosphorylation as a Negative Feedback Mechanism of TGF-Beta Signaling and a Target of Breast Cancer Therapeutics

Abstract

TGF- /Smad signaling plays crucial roles in breast cancer cell invasion and breast tumor metastasis. Understanding how TGF- signaling is regulated in metastatic breast cancer cells will allow for development of novel targeted therapy and prognostic markers. In this research, we study the mechanisms through which 2 signaling molecules, G protein-coupled receptor kinase 2 (GRK2) and Breast Cancer Anti-estrogen Resistance 3 (BCAR3), antagonize Smad signaling in breast cancer cells. We also study for correlations between expressions of these factors in breast tumors to disease outcomes. Our results advance current understanding of an important aspect of breast cancer pathology, namely TGF- -induced metastasis. They also define GRK2 and BCAR3 as novel prognostic markers of breast cancer disease relapse and metastasis.

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Document Details

Document Type
Technical Report
Publication Date
Nov 01, 2012
Accession Number
ADA571023

Entities

People

  • Jimin Guo

Organizations

  • McGill University

Tags

DTIC Thesaurus Topics

  • Biomedical Research
  • Breast Cancer
  • Cell Line
  • Cell Physiological Processes
  • Cells
  • Diseases And Disorders
  • Growth Factors
  • Kinases
  • Mammary Glands
  • Metastasis
  • Molecules
  • Neoplasms
  • Peptide Growth Factors
  • Peptides
  • Proteins
  • Resistance
  • Therapy

Fields of Study

  • Biology
  • Medicine

Readers

  • Cellular and Molecular Pathways of Apoptosis.
  • Oncology (Cancer Research).