FTO mediated glycolytic metabolism for papillary renal cell carcinoma immune evasion - 07/11/26

Abstract |
N6-methyladenosine (m6A) methylation is the predominant internal modification in eukaryotic mRNA, characterized by the methylation of adenosine at the nitrogen-6 position. A key m6A demethylase, the Fat Mass and Obesity-associated protein (FTO) play a significant role in metabolism. Renal cell carcinoma (RCC), particularly papillary RCC, is characterized by increased glucose uptake and a shift towards anaerobic glycolysis, commonly known as the “Warburg effect”. This study investigates the role of FTO in glycolytic reprogramming and immune evasion in RCC. FTO disruption resulted in a Lactate Dehydrogenase A (LDHA) expression downregulation, followed by lactate production reduction and CD8 + T cells activation. Furthermore, FTO pharmacological inhibition by DAC51 promoted CD8 + T cell activation, also resulting in increased apoptotic activity. These findings reveal a novel role for FTO in regulating tumor metabolism and immune escape in pRCC, highlighting its potential as a therapeutic target for cancer immunotherapy.
Le texte complet de cet article est disponible en PDF.Graphical Abstract |
Highlights |
• | FTO plays a crucial role in glycolytic metabolism regulation in pRCC. |
• | FTO silencing decreases LDHA expression and enhancing CD8 + T cell activation. |
• | Pharmacological inhibition of FTO promotes CD8 + T cell activation and increases apoptotic activity. |
• | Targeting FTO emerges as a potential strategy for improving cancer immunotherapy in pRCC. |
Keywords : Papillary renal cell carcinoma, M6A methylation, Glycolytic metabolism, CD8 + T cell activation , Immune evasion
Plan
Vol 204
Article 120009- novembre 2026 Retour au numéroBienvenue sur EM-consulte, la référence des professionnels de santé.
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