Hepatocyte-Specific Deletion of HIF2α Prevents NASH-Related Liver Carcinogenesis by Decreasing Cancer Cell Proliferation.


Journal

Cellular and molecular gastroenterology and hepatology
ISSN: 2352-345X
Titre abrégé: Cell Mol Gastroenterol Hepatol
Pays: United States
ID NLM: 101648302

Informations de publication

Date de publication:
2022
Historique:
received: 06 05 2021
revised: 06 10 2021
accepted: 06 10 2021
pubmed: 17 10 2021
medline: 5 4 2022
entrez: 16 10 2021
Statut: ppublish

Résumé

Hypoxia and hypoxia-inducible factors (HIFs) are involved in chronic liver disease progression. We previously showed that hepatocyte HIF-2α activation contributed significantly to nonalcoholic fatty liver disease progression in experimental animals and human patients. In this study, using an appropriate genetic murine model, we mechanistically investigated the involvement of hepatocyte HIF-2α in experimental nonalcoholic steatohepatitis (NASH)-related carcinogenesis. The role of HIF-2α was investigated by morphologic, cellular, and molecular biology approaches in the following: (1) mice carrying hepatocyte-specific deletion of HIF-2α (HIF-2α Mice carrying hepatocyte-specific deletion of HIF-2α (hHIF-2α These results indicate that the activation of HIF-2α in hepatocytes has a critical role in liver carcinogenesis during NASH progression, suggesting that HIF-2α-blocking agents may serve as novel putative therapeutic tools.

Sections du résumé

BACKGROUND & AIMS
Hypoxia and hypoxia-inducible factors (HIFs) are involved in chronic liver disease progression. We previously showed that hepatocyte HIF-2α activation contributed significantly to nonalcoholic fatty liver disease progression in experimental animals and human patients. In this study, using an appropriate genetic murine model, we mechanistically investigated the involvement of hepatocyte HIF-2α in experimental nonalcoholic steatohepatitis (NASH)-related carcinogenesis.
METHODS
The role of HIF-2α was investigated by morphologic, cellular, and molecular biology approaches in the following: (1) mice carrying hepatocyte-specific deletion of HIF-2α (HIF-2α
RESULTS
Mice carrying hepatocyte-specific deletion of HIF-2α (hHIF-2α
CONCLUSIONS
These results indicate that the activation of HIF-2α in hepatocytes has a critical role in liver carcinogenesis during NASH progression, suggesting that HIF-2α-blocking agents may serve as novel putative therapeutic tools.

Identifiants

pubmed: 34655812
pii: S2352-345X(21)00216-2
doi: 10.1016/j.jcmgh.2021.10.002
pmc: PMC8688724
pii:
doi:

Substances chimiques

Basic Helix-Loop-Helix Transcription Factors 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

459-482

Commentaires et corrections

Type : CommentIn

Informations de copyright

Copyright © 2022 The Authors. Published by Elsevier Inc. All rights reserved.

Auteurs

Beatrice Foglia (B)

Unit of Experimental Medicine and Clinical Pathology, Department of Clinical and Biological Sciences, University of Turin, Italy.

Salvatore Sutti (S)

Department of Health Sciences and Interdisciplinary Research Centre for Autoimmune Diseases, University Amedeo Avogadro of East Piedmont, Novara, Italy.

Stefania Cannito (S)

Unit of Experimental Medicine and Clinical Pathology, Department of Clinical and Biological Sciences, University of Turin, Italy.

Chiara Rosso (C)

Department of Medical Sciences, University of Turin, Torino, Italy; Division of Gastroenterology, San Giovanni Hospital, Torino, Italy.

Marina Maggiora (M)

Unit of Experimental Medicine and Clinical Pathology, Department of Clinical and Biological Sciences, University of Turin, Italy.

Riccardo Autelli (R)

Unit of Experimental Medicine and Clinical Pathology, Department of Clinical and Biological Sciences, University of Turin, Italy.

Erica Novo (E)

Unit of Experimental Medicine and Clinical Pathology, Department of Clinical and Biological Sciences, University of Turin, Italy.

Claudia Bocca (C)

Unit of Experimental Medicine and Clinical Pathology, Department of Clinical and Biological Sciences, University of Turin, Italy.

Gianmarco Villano (G)

Department of Medicine, University of Padova, Padova, Italy.

Naresh Naik Ramavath (NN)

Department of Health Sciences and Interdisciplinary Research Centre for Autoimmune Diseases, University Amedeo Avogadro of East Piedmont, Novara, Italy.

Ramy Younes (R)

Department of Medical Sciences, University of Turin, Torino, Italy; Division of Gastroenterology, San Giovanni Hospital, Torino, Italy.

Ignazia Tusa (I)

Unit of Experimental Oncology and Pathology, Department of Experimental and Clinical Biomedical Sciences, University of Florence, Florence, Italy.

Elisabetta Rovida (E)

Unit of Experimental Oncology and Pathology, Department of Experimental and Clinical Biomedical Sciences, University of Florence, Florence, Italy.

Patrizia Pontisso (P)

Department of Medicine, University of Padova, Padova, Italy.

Elisabetta Bugianesi (E)

Department of Medical Sciences, University of Turin, Torino, Italy; Division of Gastroenterology, San Giovanni Hospital, Torino, Italy.

Emanuele Albano (E)

Department of Health Sciences and Interdisciplinary Research Centre for Autoimmune Diseases, University Amedeo Avogadro of East Piedmont, Novara, Italy.

Maurizio Parola (M)

Unit of Experimental Medicine and Clinical Pathology, Department of Clinical and Biological Sciences, University of Turin, Italy. Electronic address: maurizio.parola@unito.it.

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Classifications MeSH