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UVRAG: a new player in autophagy and tumor cell growth Liang C; Feng P; Ku B; Oh BH; Jung JUAutophagy 2007[Jan]; 3 (1): 69-71Autophagy 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.|Animals[MESH]|Autophagy/*physiology[MESH]|Cell Growth Processes/*physiology[MESH]|Humans[MESH]|Neoplasms/*etiology[MESH]|Proto-Oncogene Mas[MESH]|Tumor Suppressor Proteins/*physiology[MESH] |
