| First Author | Takamura A | Year | 2011 |
| Journal | Genes Dev | Volume | 25 |
| Issue | 8 | Pages | 795-800 |
| PubMed ID | 21498569 | Mgi Jnum | J:171611 |
| Mgi Id | MGI:4950629 | Doi | 10.1101/gad.2016211 |
| Citation | Takamura A, et al. (2011) Autophagy-deficient mice develop multiple liver tumors. Genes Dev 25(8):795-800 |
| abstractText | Autophagy is a major pathway for degradation of cytoplasmic proteins and organelles, and has been implicated in tumor suppression. Here, we report that mice with systemic mosaic deletion of Atg5 and liver-specific Atg7(-/-) mice develop benign liver adenomas. These tumor cells originate autophagy-deficient hepatocytes and show mitochondrial 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. |
