Fenofibrate inhibits hypoxia-inducible factor-1 alpha and carbonic anhydrase expression through activation of AMP-activated protein kinase/HO-1/Sirt1 pathway in glioblastoma cells.


Journal

Environmental toxicology
ISSN: 1522-7278
Titre abrégé: Environ Toxicol
Pays: United States
ID NLM: 100885357

Informations de publication

Date de publication:
Dec 2021
Historique:
revised: 27 08 2021
received: 08 03 2021
accepted: 29 08 2021
pubmed: 15 9 2021
medline: 5 11 2021
entrez: 14 9 2021
Statut: ppublish

Résumé

Cancer and its associated conditions have significant impacts on public health at many levels worldwide, and cancer is the leading cause of death among adults. Peroxisome proliferator-activated receptor α (PPARα)-specific agonists, fibrates, have been approved by the Food and Drug Administration for managing hyperlipidemia. PPARα-specific agonists exert anti-cancer effects in many human cancer types, including glioblastoma (GBM). Recently, we have reported that the hypoxic state in GBM stabilizes hypoxia-inducible factor-1 alpha (HIF-1α), thus contributing to tumor escape from immune surveillance by activating the expression of the pH-regulating protein carbonic anhydrase IX (CA9). In this study, we aimed to study the regulatory effects of the PPARα agonist fibrate on the regulation of HIF-1α expression and its downstream target protein in GBM. Our findings showed that fenofibrate is the high potency compound among the various fibrates that inhibit hypoxia-induced HIF-1α and CA9 expression in GBM. Moreover, fenofibrate-inhibited HIF-1α expression is mediated by HO-1 activation in GBM cells through the AMP-activated protein kinase (AMPK) pathway. In addition, fenofibrate-enhanced HO-1 upregulation activates SIRT1 and leads to subsequent accumulation of SIRT1 in the nucleus, which further promotes HIF-1α deacetylation and inhibits CA9 expression. Using a protein synthesis inhibitor, cycloheximide, we also observed that fenofibrate inhibited HIF-1α protein synthesis. In addition, the administration of the proteasome inhibitor MG132 showed that fenofibrate promoted HIF-1α protein degradation in GBM. Hence, our results indicate that fenofibrate is a useful anti-GBM agent that modulates hypoxia-induced HIF-1α expression through multiple cellular pathways.

Identifiants

pubmed: 34520103
doi: 10.1002/tox.23369
doi:

Substances chimiques

Hypoxia-Inducible Factor 1, alpha Subunit 0
AMP-Activated Protein Kinases EC 2.7.11.31
SIRT1 protein, human EC 3.5.1.-
Sirtuin 1 EC 3.5.1.-
Carbonic Anhydrases EC 4.2.1.1
Fenofibrate U202363UOS

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

2551-2561

Subventions

Organisme : China Medical University, Taiwan
Organisme : Ministry of Science and Technology
Organisme : Taichung Tzu Chi Hospital

Informations de copyright

© 2021 Wiley Periodicals LLC.

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Auteurs

Chingju Lin (C)

Department of Physiology, School of Medicine, China Medical University, Taichung, Taiwan.

Sheng-Wei Lai (SW)

Department of Pharmacology, School of Medicine, China Medical University, Taichung, Taiwan.

Ching-Kai Shen (CK)

Graduate Institute of Biomedical Science, China Medical University, Taichung, Taiwan.

Chao-Wei Chen (CW)

Institute of New Drug Development, China Medical University, Taichung, Taiwan.

Cheng-Fang Tsai (CF)

Department of Medical Laboratory Science and Biotechnology, Asia University, Taichung, Taiwan.

Yu-Shu Liu (YS)

Department of Pharmacology, School of Medicine, China Medical University, Taichung, Taiwan.

Dah-Yuu Lu (DY)

Department of Pharmacology, School of Medicine, China Medical University, Taichung, Taiwan.
Department of Photonics and Communication Engineering, Asia University, Taichung, Taiwan.

Bor-Ren Huang (BR)

Department of Neurosurgery, Taichung Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Taichung, Taiwan.
School of Medicine, Tzu Chi University, Hualien, Taiwan.

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