The troglitazone derivative EP13 disrupts energy metabolism through respiratory chain complex I inhibition in breast cancer cells and potentiates the antiproliferative effect of glycolysis inhibitors

Date publication

avril 2024

Journal

Cancer cell international

Auteurs

Membres identifiés du Cancéropôle Est :
Dr BOISBRUN Michel , Pr FLAMENT Stéphane

Tous les auteurs :
Muller C, Lacroix-Malgras V, Kluza J, Laine W, Güler Y, Bost F, Boisbrun M, Mazerbourg S, Flament S

Lien Pubmed

https://www.ncbi.nlm.nih.gov/pubmed/38594745

Résumé

The metabolism of cancer cells generally differs from that of normal cells. Indeed, most cancer cells have a high rate of glycolysis, even at normal oxygen concentrations. These metabolic properties can potentially be exploited for therapeutic intervention. In this context, we have developed troglitazone derivatives to treat hormone-sensitive and triple-negative breast cancers, which currently lack therapeutic targets, have an aggressive phenotype, and often have a worse prognosis than other subtypes. Here, we studied the metabolic impact of the EP13 compound, a desulfured derivative of Δ2-troglitazone that we synthetized and is more potent than its parent compounds.

Mots clés

Breast cancer, Energy metabolism, Glycolysis, Mitochondria, Oxygen consumption, Thiazolidinediones, Troglitazone

Référence

Cancer Cell Int. 2024 04 10;24(1):132