Fatty Acid Synthase Activity as a Target for c-Met Driven Prostate Cancer.

摘要

The overarching goal of this project is to understand the mechanism by which fatty acid synthase (FASN) activity regulates the expression levels of the oncogenic cmet receptor tyrosine kinase in prostate cancer. My earlier work identified a connection between FASN activity and c-Met protein expression; and more recent data from this reporting period strongly suggests FASN-derived palmitate is required as a post-translation modification to c-Met in order to maintain its stability and trafficking to the plasma membrane. Conclusive evidence for this regulatory mechanism would implicate fatty acid synthase activity and/or palmitoylation as unique therapeutic targets for reducing c-Met expression.