NSD1-Mediated PPARγ Methylation Enhances PTEN Activity to Suppress Glycolysis and Tumor Progression in Endometrial Cancer - PubMed
6 hours ago
- #Epigenetics
- #Endometrial Cancer
- #Metabolism
- NSD1-mediated methylation of PPARγ at lysine 98 (K98) enhances its nuclear localization and activates PTEN transcription.
- Elevated PTEN levels suppress glycolysis, cell proliferation, and invasion in endometrial cancer (EC).
- Loss-of-function NSD1 mutations impair PPARγ methylation, leading to cytoplasmic retention and reduced PTEN expression.
- PTEN depletion increases glycolysis and drives tumor progression in EC.
- Restoring PTEN or inhibiting AKT reverses glycolytic activity and malignant phenotype caused by NSD1 deficiency.
- The study identifies an epigenetic-metabolic axis in EC, highlighting potential therapeutic targets.