Location
Georgia
Start Date
16-5-2017 1:00 PM
Description
Breast cancer is the most commonly diagnosed cancer in women worldwide. Though extensive work has been done to address the underlying mechanism of disease in order to develop novel therapeutic agents, only recently has the focus been shifted from breast cancer cells to the tumor microenvironment. Caveolin-1, a membrane protein regulating fibronectin turnover, has been directly implicated in poor prognosis when downregulated. In order to determine whether or not fibronectin works directly to downregulate caveolin-1, we plated human mammary fibroblasts on fibronectin derived from human plasma and observed changes in caveolin-1 at 24 and 48 hours. We found that fibronectin alone does not downregulate caveolin-1, and were unable to investigate any mechanism linking the two. However, TGF- β has been implicated in caveolin-1 downregulation, and it has been shown that fibronectin matrix sequesters TGF- β via LTBP-1 in the matrix. We investigated HMFs for presence of LTBP-1 via Western Blot, and found that it is expressed. Additionally, we were able to generate biological extracellular matrix for use in experiments investigating the role of ECM in concert with TGF- β in downregulating caveolin-1. We found that after 72h, biological ECM interacts with TGF-β to significantly downregulate caveolin-1 in HMFs (p
Embargo Period
6-20-2017
Analysis of the Effects of TGF-β Mediated Reduction of Caveolin-1 Expression Following Cellular Interaction with a Biological Extracellular Matrix
Georgia
Breast cancer is the most commonly diagnosed cancer in women worldwide. Though extensive work has been done to address the underlying mechanism of disease in order to develop novel therapeutic agents, only recently has the focus been shifted from breast cancer cells to the tumor microenvironment. Caveolin-1, a membrane protein regulating fibronectin turnover, has been directly implicated in poor prognosis when downregulated. In order to determine whether or not fibronectin works directly to downregulate caveolin-1, we plated human mammary fibroblasts on fibronectin derived from human plasma and observed changes in caveolin-1 at 24 and 48 hours. We found that fibronectin alone does not downregulate caveolin-1, and were unable to investigate any mechanism linking the two. However, TGF- β has been implicated in caveolin-1 downregulation, and it has been shown that fibronectin matrix sequesters TGF- β via LTBP-1 in the matrix. We investigated HMFs for presence of LTBP-1 via Western Blot, and found that it is expressed. Additionally, we were able to generate biological extracellular matrix for use in experiments investigating the role of ECM in concert with TGF- β in downregulating caveolin-1. We found that after 72h, biological ECM interacts with TGF-β to significantly downregulate caveolin-1 in HMFs (p
Comments
First-place winner of Excellence in Research - Biomedical Sciences award