Mitochondrial enzyme FAHD1 reduces ROS in osteosarcoma.


Journal

Scientific reports
ISSN: 2045-2322
Titre abrégé: Sci Rep
Pays: England
ID NLM: 101563288

Informations de publication

Date de publication:
22 Apr 2024
Historique:
received: 20 08 2023
accepted: 17 04 2024
medline: 23 4 2024
pubmed: 23 4 2024
entrez: 22 4 2024
Statut: epublish

Résumé

This study investigated the impact of overexpressing the mitochondrial enzyme Fumarylacetoacetate hydrolase domain-containing protein 1 (FAHD1) in human osteosarcoma epithelial cells (U2OS) in vitro. While the downregulation or knockdown of FAHD1 has been extensively researched in various cell types, this study aimed to pioneer the exploration of how increased catalytic activity of human FAHD1 isoform 1 (hFAHD1.1) affects human cell metabolism. Our hypothesis posited that elevation in FAHD1 activity would lead to depletion of mitochondrial oxaloacetate levels. This depletion could potentially result in a decrease in the flux of the tricarboxylic acid (TCA) cycle, thereby accompanied by reduced ROS production. In addition to hFAHD1.1 overexpression, stable U2OS cell lines were established overexpressing a catalytically enhanced variant (T192S) and a loss-of-function variant (K123A) of hFAHD1. It is noteworthy that homologs of the T192S variant are present in animals exhibiting increased resistance to oxidative stress and cancer. Our findings demonstrate that heightened activity of the mitochondrial enzyme FAHD1 decreases cellular ROS levels in U2OS cells. However, these results also prompt a series of intriguing questions regarding the potential role of FAHD1 in mitochondrial metabolism and cellular development.

Identifiants

pubmed: 38649439
doi: 10.1038/s41598-024-60012-x
pii: 10.1038/s41598-024-60012-x
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

9231

Informations de copyright

© 2024. The Author(s).

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Auteurs

Anne Heberle (A)

Institute for Biomedical Aging Research, University of Innsbruck, Innsbruck, Austria.

Elia Cappuccio (E)

Institute for Biomedical Aging Research, University of Innsbruck, Innsbruck, Austria.

Andreas Andric (A)

Institute for Biomedical Aging Research, University of Innsbruck, Innsbruck, Austria.

Tatjana Kuen (T)

Institute for Biomedical Aging Research, University of Innsbruck, Innsbruck, Austria.

Anna Simonini (A)

Institute for Biomedical Aging Research, University of Innsbruck, Innsbruck, Austria.

Alexander K H Weiss (AKH)

Institute for Biomedical Aging Research, University of Innsbruck, Innsbruck, Austria. alexander.weiss@uibk.ac.at.

Classifications MeSH