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Autophagy represses hepatic carcinogenesis

Hepatocyte-specific knockout of the essential autophagy gene Autophagy-related 7 (Atg7) is sufficient to cause hepatic carcinogenesis. A recent paper by Lee et al. unveils the molecular pathway accounting for hepatic hypertrophy and hyperplasia followed by malignant transformation. This pathway invo...

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Detalles Bibliográficos
Autores principales: Paillet, Juliette, Kroemer, Guido
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Taylor & Francis 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6548487/
https://www.ncbi.nlm.nih.gov/pubmed/31211229
http://dx.doi.org/10.1080/23723556.2019.1573080
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author Paillet, Juliette
Kroemer, Guido
author_facet Paillet, Juliette
Kroemer, Guido
author_sort Paillet, Juliette
collection PubMed
description Hepatocyte-specific knockout of the essential autophagy gene Autophagy-related 7 (Atg7) is sufficient to cause hepatic carcinogenesis. A recent paper by Lee et al. unveils the molecular pathway accounting for hepatic hypertrophy and hyperplasia followed by malignant transformation. This pathway involves the overactivation of the transcription factor yes-associated protein (YAP), which turns out to be an autophagic substrate. Of note, the transcriptional signature activated in mouse hepatocytes lacking Atg7 resembles that found in non-alcoholic steatohepatitis (NASH), as well as in the steatohepatitic subtype of human hepatocellular carcinomas.
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spelling pubmed-65484872020-05-13 Autophagy represses hepatic carcinogenesis Paillet, Juliette Kroemer, Guido Mol Cell Oncol Review Hepatocyte-specific knockout of the essential autophagy gene Autophagy-related 7 (Atg7) is sufficient to cause hepatic carcinogenesis. A recent paper by Lee et al. unveils the molecular pathway accounting for hepatic hypertrophy and hyperplasia followed by malignant transformation. This pathway involves the overactivation of the transcription factor yes-associated protein (YAP), which turns out to be an autophagic substrate. Of note, the transcriptional signature activated in mouse hepatocytes lacking Atg7 resembles that found in non-alcoholic steatohepatitis (NASH), as well as in the steatohepatitic subtype of human hepatocellular carcinomas. Taylor & Francis 2019-05-13 /pmc/articles/PMC6548487/ /pubmed/31211229 http://dx.doi.org/10.1080/23723556.2019.1573080 Text en © 2019 The Author(s). Published with license by Taylor & Francis Group, LLC. http://creativecommons.org/licenses/by-nc-nd/4.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives License (http://creativecommons.org/licenses/by-nc-nd/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited, and is not altered, transformed, or built upon in any way.
spellingShingle Review
Paillet, Juliette
Kroemer, Guido
Autophagy represses hepatic carcinogenesis
title Autophagy represses hepatic carcinogenesis
title_full Autophagy represses hepatic carcinogenesis
title_fullStr Autophagy represses hepatic carcinogenesis
title_full_unstemmed Autophagy represses hepatic carcinogenesis
title_short Autophagy represses hepatic carcinogenesis
title_sort autophagy represses hepatic carcinogenesis
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6548487/
https://www.ncbi.nlm.nih.gov/pubmed/31211229
http://dx.doi.org/10.1080/23723556.2019.1573080
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