RESEARCH COMMUNICATION Autophagy-deficient mice

Autophagy is a major pathway for degradation of cyto-plasmic proteins and organelles, and has been implicated in tumor suppression. Here, we report that mice with systemic mosaic deletion of Atg5 and liver-specificAtg7/ mice develop benign liver adenomas. These tumor cells originate autophagy-deficient hepatocytes and show mito-chondrial swelling, p62 accumulation, and oxidative stress and genomic damage responses. The size of the Atg7/ liver tumors is reduced by simultaneous deletion of p62. These results suggest that autophagy is important for the suppression of spontaneous tumorigenesis through a cell-intrinsic mechanism, particularly in the liver, and that p62 accumulation contributes to tumor progression. Supplemental material is available for this article. Received December 23, 2010; revised version accepte