Mechanism of RhoB/FTI Action in Breast Cancer
Abstract
In January 2002 the laboratory of the principal investigator's mentor relocated from The Wistar Institute to the Lankenau Institute for Medical Research (LIMFI). Due to this move, as well as the departure of the principal investigator (postdoctoral fellow) from the mentor's research group, transfer of this DoD postdoctoral grant to a new principle investigator is only just now being completed. As a result, limited progress was made during 8 months of the 12 month period covered by this progress report. Aim 1 involving mouse genetics experiments are currently on hold and no new progress is reported. However, in Aim 2, we obtained positive evidence of a role for RhoB and its effector kinase PRK in the antiproliferative action of FTI in rat epithelial and fibroblast cell model systems. Briefly, we demonstrated that RhoB could phenocopy the antiproliferative response to FTI in epithelial cells transformed by activated K-Ras or Racl oncogenes, and by using effector mutants of RhoB, we obtained evidence that interactions between RhoB and PRK kinase is involved in this effect. Similarly, manipulating PRK level, localization, or activity in H-Ras-transformed fibroblasts altered the FTI response. This work has been accepted for publication and is currently in press at Oncogene.
Document Details
- Document Type
- Technical Report
- Publication Date
- May 01, 2002
- Accession Number
- ADA412302
Entities
People
- George C. Prendergast
- Neena S. Rane
Organizations
- University of Pennsylvania