Fig. 7

Schematic presentation of how cholesterol flux inhibitors affect cholesterol balance in PDAC cells and the impact of fatty acids. Intracellular cholesterol flux can be blocked at the levels of by inhibition of cholesterol synthesis (HMGCR-i), cholesterol esterification (SOAT1-i), and CE lipolysis (NCEH1-i). In addition, inhibition of HSL/MGLL (HSL/MGLL-i) reduces FA availability. Disturbed cholesterol flux leads to increased cholesterol burden, which alters PDAC cell behavior. FA improves the intracellular cholesterol balance and counteracts the effects of cholesterol flux inhibition in PDAC cells. CE cholesteryl ester, FA fatty acids, HMGCR 3-Hydroxy-3-Methylglutaryl-CoA reductase, HSL hormone-sensitive lipase, MGLL monoacylglycerol lipase, NCEH1 neutral cholesterol ester hydrolase 1, SOAT1 sterol O-acyltransferase 1, TAG triacylglycerol