UVRAG: A NEW PLAYER IN AUTOPHAGY AND TUMOR CELL GROWTH

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This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Autophagy has a well-documented role in the maintenance of homeostasis and the response to stressful environment and it is often deregulated in various human diseases including cancer. The regulation of the Beclin1-PI3KC3 complex lipid kinase activity is the critical element in autophagy signaling pathway. Previous studies1have demonstrated that Beclin1-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 Beclin1-dependent autophagy. UVRAG interacts with Beclin1, leading to activation of autophagy and thereof inhibition of tumorigenesis.