The Role of c-Src Activation in Prostate Tumor Progression
Abstract
DOD Award number DAMD17-03-l-0484, "The Role of c-Src Activation in Prostate Tumor Progression", has as its goal an understanding of the mechanisms of how activation of the protein tyrosine kinase, Src, contributes to prostate tumor progression and how Src regulation in host osteoclasts regulates metastatic growth of prostate tumor cells in the bone. In the first year of work, we developed cell line models required for these studies. Using these cells, we demonstrated that increased Src activity leads to increased expression of vascular endothelial growth factor (VEGF) through a specific transcriptional mechanism involving Src activation of STAT3. We further demonstrate that Src activation leads directly to increased lymph node metastases in orthotopic nude mouse models. These data led to a publication on how Src promotes prostate tumor metastasis. To examine the role of Src in growth of prostate tumor cells in the bone, we have now developed a Src-/- nu/nu strain of mice. Further breeding of these mice is required for tumor studies. Continued studies should provide new insights into role of Src in both the tumor and host environment in promoting prostate tumor cell metastasis.
Document Details
- Document Type
- Technical Report
- Publication Date
- Jul 01, 2005
- Accession Number
- ADA442637
Entities
People
- Gary E. Gallick
Organizations
- The University of Texas MD Anderson Cancer Center