The study by Parejo-Alonso et al. identifies PPAR-δ as a critical transcription factor mediating pancreatic cancer cell adaptation to microenvironmental stress.

Normally involved in lipid metabolism, PPAR-δ is overexpressed in pancreatic tumors and, under metabolic stress, senses lipidomic alterations, triggering metabolic reprogramming that enhances glycolysis and promotes a pro-invasive phenotype.

In vitro and in vivo models confirm that pharmacological inhibition of PPAR-δ reverses these adaptations and reduces metastatic potential, highlighting its relevance as a promising therapeutic target for pancreatic cancer treatment.

Complete information at the following link: https://pubmed.ncbi.nlm.nih.gov/40607925/