Supplementary Figures 1-6, Tables 1-4 from DUSP1 Expression Induced by HDAC1 Inhibition Mediates Gefitinib Sensitivity in Non–Small Cell Lung Cancers

Figure S1. The effect of gefitinib on gefitinib-resistant NSCLC cells. Figure S2. Knockdown of HDAC1 in PC9/IR and HCC827/IR cells restored gefitinib sensitivity. Figure S3. Novel HDAC inhibitors WJ compounds inhibited cell growth and induced acetylation of histone-H3 and α-tubulin in various cancer cells. Figure S4. Synergistic effect of WJ-26210-2 in combination with gefitinib on cell viability and apoptotic markers in gefitinib-resistant NSCLC cells. Figure S5. DUSP1 was induced in gefitinib-resistant cells by combination treatment and knockdown of it conferred gefitinib resistance in gefitinib-sensitive cells. Figure S6. Combination of HDAC1 inhibition and gefitinib induced in vivo DUSP1 expression in H1975 cells and inhibited lung cancer growth. Table S1. IC50 value for the inhibition of HDACs by WJ compounds and SAHA. Table S2. IC50 and CI values for the antiproliferative effects of gefitinib, WJ-26210-2 and SAHA alone or combination on the growth of NSCLC cells. Table S3. Effect of combination of gefitinib and WJ-26210-2 on RT2 Profiler PCR-array in gefitinib-resistant cells. Table S4. The DUSP1/TBP ratio of malignant pleura effusions of NSCLC patients.