FGFR4 Downregulation of Cell Adhesion in Prostate Cancer
Annual rept. 1 Mar 2007-29 Feb 2008
CALIFORNIA UNIV SAN DIEGO LA JOLLA
Pagination or Media Count:
We have been successful in creating the necessary constructs for generating prostate cancer cells inducible for FGFR4. Despite our best efforts, however, we have not been able to successfully incorporate the pVgRXR regulatory plasmid into prostate cancer cells. We proceeded by transiently transfecting PC3 prostate cancer cells to look at effects on downstream signaling components and found no significant differences in MAPK activity, NCAM expression or STAT1 and STAT5 localization when comparing the various FGFR4 constructs, including FL-FGFR4 and PTD-FGFR4. We have also made a very exciting discovery recently that may be important for understanding the role of FGFR4 in prostate cancer progression. Using a yeast-two-hybrid assay, we found that FGFR4 interacts with IKKbeta and leads to its tyrosine phosphorylation. We are currently investigating if there are any differences in binding tyrosine phosphorylation with the G388R polymorphism. Though not specifically relating to cell adhesion, understanding the role of FGFR4 in altering IKKbeta activity may be important for our understanding of prostate cancer progression.
- Genetic Engineering and Molecular Biology
- Medicine and Medical Research