Pancreatic cancer lipid signaling network

Pancreatic ductal adenocarcinoma exhibits a profound rewiring of lipid metabolism, with fatty acids, cholesterol, phosphoinositides, and sphingolipids sustaining tumor growth, survival, metabolic plasticity, and metastatic dissemination. 

Lipid species act as potent signaling mediators that integrate with oncogenic KRAS, phosphoinositide 3-kinase – AKT–mechanistic target of rapamycin complex 1, and WNT pathways, reshaping proliferation, migration, and stress adaptation.

Tumor–stroma interactions provide essential lipids through cancerassociated fibroblast-derived autotaxin–lysophosphatidic acid signaling, altered cholesterol trafficking, and nutrient scavenging pathways such as macropinocytosis.

Lipid-driven adaptive programs promote resistance to chemotherapy, KRAS inhibitors, and metabolic stress, revealing druggable vulnerabilities across biosynthetic, uptake, and lipid signaling nodes.

https://www.cell.com/trends/endocrinology-metabolism/fulltext/S1043-2760(26)00065-2

https://sciencemission.com/Lipid-signaling-networks-in-pancreatic-cancer