Supplementary Data, Tables 1-7, Supplementary Figures 1-11 from Secreted Factors from Adipose Tissue Reprogram Tumor Lipid Metabolism and Induce Motility by Modulating PPARα/ANGPTL4 and FAK

Abstract

<p>Table S1: Primersequences used for human and murine cell lines. Table S2: Upstream regulators of genes with increased expression in MDA-MB-231 cells co-cultured with murine adipose tissue (HFD). Table S3: Upstream regulators of genes with decreased expression in MDA-MB-231 cells co-cultured with murine adipose tissue (HFD). Table S4: Characterization of the free fatty acid profile of ACMs<30 and ACMs>40. Table S5: Enriched GO terms (Biological Process) in genes with {greater than or equal to}1.5-fold downregulation in MDAMB-231 cells co-cultured with adipose tissue of HFD mice vs control. Table S6: Enriched GO terms (Biological Process) in genes with {greater than or equal to}1.5-fold upregulation in MDA-MB231 cells co-cultured with adipose tissue of HFD mice vs control. Fig. S1: Pathway Analysis and gene expression data of co-cultured MDA-MB-231 cells. Fig. S2: ACM increases PPAR target gene expression in murine E0771 cells. Fig. S3: ANGPTL4 mRNA is increased in human triple negative breast cancer and associated with reduced survival. Fig. S4: PPAR target gene expression is dependent on PPARα. Fig. S5: Free fatty acids activate PPAR signaling in TNBC cells. Fig. S6: Incubation of TNBC cells with ACM or BSA-OA decreases de novo FA synthesis. Fig. S7: Cultivation of TNBC cells with ACM or BSA-OA induces the expression of β-oxidation genes. Fig. S8: Treatment with oleic acid increases intracellular lipid droplet formation in TNBC cells. Fig S9: ACM promotes proliferation and migration of E0771 cells. Fig. S10: ANGPTL4 knockdown in MDA-MB-231 cells does not affect cell proliferation. Fig. S11: MMP2 is upregulated in MDA-MB-231 cells upon ACM cultivation.</p>