期刊
GENES & DEVELOPMENT
卷 25, 期 8, 页码 795-800出版社
COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
DOI: 10.1101/gad.2016211
关键词
autophagy; tumorigenesis; model mouse; oxidative stress
资金
- Ministry of Education, Culture, Sports, Science, and Technology, Japan
- Funding Program for Next Generation World-Leading Researchers
- Takeda Science Foundation
- Japanese Society of Anti-Aging Medicine
- Grants-in-Aid for Scientific Research [21000012, 21659045] Funding Source: KAKEN
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.
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