UVRAG: a new player in autophagy and tumor cell growth.
Autophagy has a well-documented role in the maintenance of homeostasis and the response to stressful environments and it is often deregulated in various human diseases including cancer. The regulation of the Beclin 1-PI3KC3 complex lipid kinase activity is a critical element in the autophagy signaling pathway. Previous studies(1) have demonstrated that Beclin 1-PI3KC3-mediated autophagy is negatively regulated by a proto-oncogene Bcl-2. We have recently identified a novel coiled-coil UVRAG tumor suppressor candidate, which positively engages in Beclin 1-dependent autophagy. UVRAG interacts with Beclin 1, leading to activation of autophagy and thereof inhibition of tumorigenesis. This finding adds a new player to the emerging picture of the autophagy network, under-scoring the importance of the coordinated activity between Bcl-2 and UVRAG in the regulation of Beclin 1-PI3KC3-mediated autophagy and tumor cell control.
Liang
Chengyu
C
Department of Microbiology and Molecular Genetics and Tumor Virology Division, New England Primate Research Center, Harvard Medical School, 1 Pine Hill Drive, Southborough, MA 01772, USA.
Feng
Pinghui
P
Ku
Bonsu
B
Oh
Byung-Ha
BH
Jung
Jae U
JU
D000818:Animals; D001343:Autophagy / Q000502:physiology*; D048708:Cell Growth Processes / Q000502:physiology*; D006801:Humans; D009369:Neoplasms / Q000209:etiology*; D000090063:Proto-Oncogene Mas; D025521:Tumor Suppressor Proteins / Q000502:physiology*
C000715470:MAS1 protein, human; D000090063:Proto-Oncogene Mas; D025521:Tumor Suppressor Proteins; C408122:UVRAG protein, human