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
Annual summary rept. 1 Nov 2011-31 Oct 2012
MCGILL UNIV HEALTH CENTER MONTREAL (QUEBEC)
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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.
- Medicine and Medical Research