The role of altered lipid metabolism in pancreatic ductal adenocarcinoma (PDAC) is poorly appreciated. We recently identified the lipid signature of PDAC and revealed low-density lipoprotein receptor (Ldlr) as a metabolic driver of this disease. Here, we comment our findings that disruption of Ldlr leads to intratumoral cholesterol imbalance and improves chemotherapy efficiency.
Keywords: Cholesterol; Ldlr; gemcitabine; mechanisms of oncogenesis and tumor progression; metabolism; novel therapeutic targets; pancreatic cancer; tumor metabolism.