E2F1 and E2F2-Mediated Repression of CPT2 Establishes a Lipid-Rich Tumor-Promoting Environment.

Animals Carcinogens Carcinoma, Hepatocellular / etiology Carnitine O-Palmitoyltransferase / antagonists & inhibitors Diet, High-Fat / adverse effects E2F1 Transcription Factor / genetics E2F2 Transcription Factor / genetics Gene Expression Regulation Lipids / analysis Liver Neoplasms / etiology Male Mice Mice, Inbred C57BL Mice, Knockout Non-alcoholic Fatty Liver Disease / complications Prognosis Promoter Regions, Genetic

Journal

Cancer research

ISSN: 1538-7445

Titre abrégé: Cancer Res

Pays: United States

ID NLM: 2984705R

Informations de publication

Date de publication:
01 06 2021

Historique:

received: 16 06 2020

revised: 15 12 2020

accepted: 24 03 2021

pubmed: 28 3 2021

medline: 5 11 2021

entrez: 27 3 2021

Statut: ppublish

Résumé

Lipid metabolism rearrangements in nonalcoholic fatty liver disease (NAFLD) contribute to disease progression. NAFLD has emerged as a major risk for hepatocellular carcinoma (HCC), where metabolic reprogramming is a hallmark. Identification of metabolic drivers might reveal therapeutic targets to improve HCC treatment. Here, we investigated the contribution of transcription factors E2F1 and E2F2 to NAFLD-related HCC and their involvement in metabolic rewiring during disease progression. In mice receiving a high-fat diet (HFD) and diethylnitrosamine (DEN) administration,

Identifiants

DOI: 10.1158/0008-5472.CAN-20-2052 PMID: 33771899

pubmed: 33771899

pii: 0008-5472.CAN-20-2052

doi: 10.1158/0008-5472.CAN-20-2052

doi:

Substances chimiques

Carcinogens 0

E2F1 Transcription Factor 0

E2F1 protein, human 0

E2F2 Transcription Factor 0

E2F2 protein, human 0

Lipids 0

Carnitine O-Palmitoyltransferase EC 2.3.1.21

Types de publication

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

Langues

eng

Sous-ensembles de citation

Pagination

2874-2887

Informations de copyright

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