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Quach, Christine; Song, Ying; Guo, Hongrui; Li, Shun; Maazi, Hadi; Fung, Marshall; Sands, Nathaniel; O'Connell, Douglas; Restrepo-Vassalli, Sara; Chai, Billy; Nemecio, Dali; Punj, Vasu; Akbari, Omid; Idos, Gregory E; Mumenthaler, Shannon M; Wu, Nancy; Martin, Sue Ellen; Hagiya, Ashley; Hicks, James; Cui, Hengmin; Liang, Chengyu
Nature communications, 12/2019, Volume: 10, Issue: 1Journal Article
Aberrant autophagy is a major risk factor for inflammatory diseases and cancer. However, the genetic basis and underlying mechanisms are less established. UVRAG is a tumor suppressor candidate involved in autophagy, which is truncated in cancers by a frameshift (FS) mutation and expressed as a shortened UVRAG . To investigate the role of UVRAG in vivo, we generated mutant mice that inducibly express UVRAG (iUVRAG ). These mice are normal in basal autophagy but deficient in starvation- and LPS-induced autophagy by disruption of the UVRAG-autophagy complex. iUVRAG mice display increased inflammatory response in sepsis, intestinal colitis, and colitis-associated cancer development through NLRP3-inflammasome hyperactivation. Moreover, iUVRAG mice show enhanced spontaneous tumorigenesis related to age-related autophagy suppression, resultant β-catenin stabilization, and centrosome amplification. Thus, UVRAG is a crucial autophagy regulator in vivo, and autophagy promotion may help prevent/treat inflammatory disease and cancer in susceptible individuals.
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