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Fig. 2 | Cancer Cell International

Fig. 2

From: Fatty acids abrogate the growth-suppressive effects induced by inhibition of cholesterol flux in pancreatic cancer cells

Fig. 2

Effect of selected lipid flux inhibitors on PDAC cell viability, proliferation, and cell density. A. A schematic presentation of lipid turnover through LDs, the key enzymes, and corresponding inhibitors. B-D. PDAC cells were incubated in DMEM supplemented with 1% FBS and various inhibitors (10 µM for HSL/MGLL-i and NCEH1-i, 5 µM for SOAT1-i and HMGCR-i) for 48 h. B. Cell viability assessed by the percentage of propidium iodide (PI) positive (non-viable) cells relative to Hoechst 33342 positive (total) cells. C. Cell proliferation assessed by BrdU incorporation. D. Relative cell density assessed by crystal violet staining. Results are presented as means ± SD (n = 4–5, *p < 0.05 comparing inhibitors with DMSO). ATGL adipose triacylglycerol lipase, CE cholesteryl ester, DAG diacylglycerol, DGATs diacylglycerol O-Acyltransferases, FC free cholesterol, FFA free fatty acids, HMGCR 3-Hydroxy-3-Methylglutaryl-CoA reductase, HSL hormone-sensitive lipase, LAL lysosomal acid lipase, LD lipid droplet, MAG monoacylglycerol, MGLL monoacylglycerol lipase, NCEH1 neutral cholesterol ester hydrolase 1, SOAT1 sterol O-acyltransferase 1, TAG triacylglycerol

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