Supplementary table 2.xlsx

<p><b>Lipidomic data </b> <b></b></p><p>Lipidomic maps were generated for mouse KGC pancreatic tumor organoid lines expressing doxycycline-inducible constitutively-active<b> </b>mutant GNAS (GNAS^R201C). The organoids were analyzed in the presence of doxycycline; Dox(+) or absence of doxycycline; Dox(-). LC-MS experiments for non-polar metabolites were performed using a KCG organoid line in triplicate for the +Dox and -Dox conditions and denoted as Dox(+)-1; Dox(+)-2; Dox(+)-3; Dox(-)-1; Dox(-)-2; Dox(-)-3. LC-MS/MS-based lipidomic experiments and data analyses were performed as described in the reference¹. The data were normalized to the total number of cells in the organoids from replicate wells. Metabolites were quantified by integrating the area under the curve. Lipidation (lipid species detected); Class (class of lipids. see lipid keys in the document)</p><p>Reference: 1) Smulan, L. J.<i>et al.</i>Cholesterol-Independent SREBP-1 Maturation Is Linked to ARF1 Inactivation. <i>Cell reports</i><b>16</b>, 9-18, doi:10.1016/j.celrep.2016.05.086 (2016).</p

Supplementary table 3

<p><b>Polar metabolite data</b></p><p>Polar metabolite profiling data were generated for a mouse KGC pancreatic tumor line expressing doxycycline-inducible constitutively-active<b> </b>mutant GNAS (GNAS^R201C) growing in 2D culture in the presence of doxycycline; Dox(+) or absence of doxycycline; Dox(-). The cells were harvested as 5 biological replicates and flash-frozen. The polar metabolites were extracted with 40:40:20 acetonitrile/methanol/water and replicates are denoted as Dox(+)-1, Dox(+)-2, Dox(+)-3, Dox(+)-4, Dox(+)-5 and Dox(-)-1, Dox(-)-2, Dox(-)-3, Dox(-)-4, Dox(-)-5. Polar metabolites were analyzed by QQQ-LC/MS/MSas described in the reference^1.The ion counts were normalized to the total cell number. Metabolites were quantified by integrating the area under the curve, and then normalized to internal standard values. </p><p> </p><p>1) Louie, S. M.<i>et al.</i>GSTP1 Is a Driver of Triple-Negative Breast Cancer Cell Metabolism and Pathogenicity. <i>Cell Chem Biol</i><b>23</b>, 567-578, doi:10.1016/j.chembiol.2016.03.017 (2016). </p