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*

*この研究の対応する著者

研究成果: Article査読

892 被引用数 (Scopus)

抄録

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.

本文言語English
ページ(範囲)795-800
ページ数6
ジャーナルGenes and Development
25
8
DOI
出版ステータスPublished - 2011 4月 15
外部発表はい

ASJC Scopus subject areas

  • 遺伝学
  • 発生生物学

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