Abstract:
:Activation of the Hippo pathway effector Yap underlies many liver cancers, however no germline or somatic mutations have been identified. Autophagy maintains essential metabolic functions of the liver, and autophagy-deficient murine models develop benign adenomas and hepatomegaly, which have been attributed to activation of the p62/Sqstm1-Nrf2 axis. Here, we show that Yap is an autophagy substrate and mediator of tissue remodeling and hepatocarcinogenesis independent of the p62/Sqstm1-Nrf2 axis. Hepatocyte-specific deletion of Atg7 promotes liver size, fibrosis, progenitor cell expansion, and hepatocarcinogenesis, which is rescued by concurrent deletion of Yap. Our results shed new light on mechanisms of Yap degradation and the sequence of events that follow disruption of autophagy, which is impaired in chronic liver disease.
journal_name
Nat Communjournal_title
Nature communicationsauthors
Lee YA,Noon LA,Akat KM,Ybanez MD,Lee TF,Berres ML,Fujiwara N,Goossens N,Chou HI,Parvin-Nejad FP,Khambu B,Kramer EGM,Gordon R,Pfleger C,Germain D,John GR,Campbell KN,Yue Z,Yin XM,Cuervo AM,Czaja MJ,Fiel MI,Hoshdoi
10.1038/s41467-018-07338-zsubject
Has Abstractpub_date
2018-11-23 00:00:00pages
4962issue
1issn
2041-1723pii
10.1038/s41467-018-07338-zjournal_volume
9pub_type
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