Supplementary Figures S1-S8; Supplementary Tables S1-S8; Supplementary methods from <i>De Novo</i> Lipid Synthesis Facilitates Gemcitabine Resistance through Endoplasmic Reticulum Stress in Pancreatic Cancer

Figure S1: FASN inhibition with orlistat shows synergistic activity with gemcitabine in AsPC-1 cells; Figure S2: Effect of orlistat on the lipid content of pancreatic cancer cells; Figure S3: Platensimycin shows synergistic activity with gemcitabine in AsPC-1 cells; Figure S4: Lipid synthesis inhibitor C75 improves the effect of gemcitabine in pancreatic cancer cell lines; Figure S5: Lipid synthesis inhibitor fatostatin improves the effect of gemcitabine in pancreatic cancer cell lines; Figure S6: Albumin-conjugated palmitate does not rescue the anti-proliferative effects of gemcitabine; Figure S7: AdCM does not rescue the antiproliferative effect of gemcitabine on pancreatic cancer cells under the regular and stress conditions; Figure S8: Effect of AdCM on the lipid content of pancreatic cancer cells. Table S1: Metabolic pathway enrichment in pancreatic ductal adenocarcinoma patients treated with gemcitabine (data pooled from TCGA); Table S2: Patient Characteristics for Figure 1D; Table S3: Cell line gemcitabine responsiveness (IC50), FASN expression, and mutation status; Table S4: Orlistat responsiveness in pancreatic cancer cell lines; Table S5: Combination index of gemcitabine and orlistat in pancreatic cancer cell lines PANC-1, AsPC-1, Capan-1, and HPAF-II; Table S6: Combination index of gemcitabine and C75 in pancreatic cancer cell lines PANC-1, and AsPC-1; Table S7: Combination index of gemcitabine and fatostatin in pancreatic cancer cell lines PANC-1, and AsPC-1; Table S8: Combination index of gemcitabine and thapsigargin in pancreatic cancer cell lines PANC-1. SUPPLEMENTARY MATERIALS AND METHODS