Beta-catenin/TCF Signaling and Castrate-Resistant Progression of Osteoblastic Bone Metastases
Authors
Navone NM
Institution
University of Texas, M.D. Anderson Cancer Center, Houston
Country
United States
Year
2009
Journal
Storming Media – Report
Abstract
In this project, we are studying the role of D32G-mutant beta-catenin in the expression of secretory genes by prostate cancer cells. We believe that D32G-mutant beta-catenin potently activates a subset of beta-catenin/wnt downstream target genes, thus providing a tool for identifying “bone progression” factors activated by this pathway in prostate cancer. Results from the studies performed during this period indicate that activation of beta-catenin in prostate cancer cells stimulates a subset of beta-catenin target genes and suggest that beta-catenin expression in prostate cancer cells mediates the prostate cancer–induced new bone formation in vitro and in vivo. These results provide confidence that our gene-expression studies will be informative for identifying the beta-catenin downstream target genes that mediate the osteoblastic phenotype induced by prostate cancer cells. Immunohistochemical studies performed in human bone metastases of prostate cancer identified 4 groups based on beta-catenin intracellular distribution and expression and androgen receptor expression. It will be interesting to assess how the selected factors induced by beta-catenin in prostate cancer cells are expressed in the different groups. Although these results would only be correlative, they would provide the basis for prioritization in future studies.
Product use
Isolation and cultivation for transient transfection of siRNA and lentiviral-mediated shRNA expression; total RNA isolation and quantitative RT-PCR; comparative gene array analysis "We have observed that MDA PCa 118b cells can be cultured in CnT-52 medi
Tissue type
Prostate
Tissue info
MDA PCa 118b cells isolated from subcutaneous prostate tumors developed in SCID mice