Fig. 6

GR-28 exhibits synergy with fatty acid metabolism inhibitor in high-REST GBM cells. A–C Drug combination landscapes (72 h) in GBMs (A–B) and HepG2 cells (C). HepG2 cells were treated under the same doses as A172. Shown is the representative landscape having maximal synergy score closest to its mean value. Landscapes were built using “synergyfinder” R package (Bliss model). D Low-toxic dose of Triacsin C sensitizes high-REST GBM cells to GR-28. Shown are viability rates (mean ± SEM) normalized to that of solvent-control wells derived from three independent experiments, n = 9. E Maximal synergy scores (mean ± SEM) extracted from three independent drug combination landscapes (GR-28/Triacsin C) in A172, T98G, and HepG2 cells. Statistical difference was tested using a t-test. Individual data values are provided in Additional File 10P. F Selective effect of GR-28/Triacsin C drug combination on GBM cells. Plotted are viabilities (mean ± SEM, 3 independent experiments, n = 9–12, 72 h) normalized to that of solvent-control wells under single drug treatments and combination treatments. Statistical difference was tested using multiple t-tests. G Simultaneous targeting of REST and fatty acid metabolism results in synergistic cell death in GBM cells. Model was created using BioRender software. **p < 0.01; *p < 0.05