The isopeptidase USP2a regulates the stability of fatty acid synthase in prostate cancer.

摘要: Cellular levels of key regulatory proteins are controlled via ubiquitination and subsequent degradation. Deubiquitinating enzymes or isopeptidases can potentially prevent targeted destruction protein substrates through deubiquitination prior to proteasomal However, only one deubiquitinating enzyme date has been matched a specific substrate in mammalian cells shown functionally modify it. Here we show that the isopeptidase USP2a (ubiquitin-specific protease-2a) interacts with stabilizes fatty acid synthase (FAS), which is often overexpressed biologically aggressive human tumors. Further, androgen-regulated prostate cancer, its functional inactivation results decreased FAS enhanced apoptosis. Thus, plays critical role cancer cell survival stabilization represents therapeutic target cancer.