Autophagy-deficient mice develop multiple liver tumors

Akito Takamura, Masaaki Komatsu, Taichi Hara, Ayako Sakamoto, Chieko Kishi, Satoshi Waguri, Yoshinobu Eishi, Okio Hino, Keiji Tanaka, Noboru Mizushima*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

1030 Citations (Scopus)


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 cellintrinsic mechanism, particularly in the liver, and that p62 accumulation contributes to tumor progression.

Original languageEnglish
Pages (from-to)795-800
Number of pages6
JournalGenes and Development
Issue number8
Publication statusPublished - 2011 Apr 15
Externally publishedYes


  • Autophagy
  • Model mouse
  • Oxidative stress
  • Tumorigenesis

ASJC Scopus subject areas

  • Genetics
  • Developmental Biology


Dive into the research topics of 'Autophagy-deficient mice develop multiple liver tumors'. Together they form a unique fingerprint.

Cite this