Supplementary Figures 1 - 8 from The SMARCA2/4 ATPase Domain Surpasses the Bromodomain as a Drug Target in SWI/SNF-Mutant Cancers: Insights from cDNA Rescue and PFI-3 Inhibitor Studies

Abstract

Figure S1. Genomic analysis of SWI/SNF alterations in human cancer. Figure S2. SMARCA4-deficient lung cancer cells depend on SMARCA2 expression for growth. Figure S3. In-situ cell extraction assay for PFI-3 treatment. Figure S4. SMARCA2/4 bromodomain inhibitor does not alter growth of lung cancer cells. Figure S5. Analysis of SMARCA4 target gene expression and promoter occupancy following prolonged treatment with PFI-3. Figure S6. Pharmacological PFI-3 inhibitor studies in leukemia cells. Figure S7. Pharmacological EZH2 inhibitor studies. Figure S8. Genome-wide microarray analysis of SMARCA2 knockdown in A549 cells reconstituted with SMARCA4 cDNAs. Table S1: Survey of genomic lesions in SWI/SNF across different cancer types. Table S2: Sequence information of shRNA's and siRNA's used in the study. Table S3. BROMOScan (DiscoveRx) profiling of PFI-3 (at 2uM) against 32 bromodomains. Table S4. Definition of gene sets (i.e. SMARCA2 knockdown signatures) from SMARCA4 rescue experiments in A549 cells. Table S5. Summary of GSEA normalized enrichment scores (NES) and false discovery rate (FDR) for rescue experiment using ATP-Dead, BRD-Mut and vector control and compared to WT.