Supplementary Figures S1 - S8, Tables S1 - S9 from Targeting p300 Addiction in CBP-Deficient Cancers Causes Synthetic Lethality by Apoptotic Cell Death due to Abrogation of MYC Expression

Supplementary Figure S1. Identification of the p300 gene as a synthetic lethal hit. Supplementary Figure S2. Identification of MYC as a key factor in determining cancer cell survival under p300 depletion in CBP-KO cells or CBP depletion in p300-KO cells. Supplementary Figure S3. MYC transcriptional initiation is inactivated by suppression of histone H3K18/K27 acetylation upon p300 depletion in CBP-deficient cancer cells. Supplementary Figure S4. p300 depletion is lethal in cancer cells harboring loss-offunction mutations in CBP. Supplementary Figure S5. Response of CBP-deficient lung cancer cells to the p300 HAT inhibitor C646. Supplementary Figure S6. Depletion or inhibition of p300 suppresses growth of hematopoietic cancers with loss-of-function mutation of CBP. Supplementary Figure S7. Effect to BRD4 localization in the MYC locus in p300 depletion in CBP-deficient cancer cells. Supplementary Figure S8. CBP/CREBBP and p300/EP300 aberrations and known druggable aberrations of FGFR1 or ERBB2 amplification in lung squamous cell carcinomas and stomach adenocarcinomas. Supplementary Table S1. Raw data of survival fraction in siRNA screen. Supplementary Table S2. The top13 statistically significant pathways obtained from WikiPathways analysis. Supplementary Table S3. Genes commonly involved in the 13 functional pathways. Supplementary Table S4. CBP and p300 mutations in a variety of cancers. Supplementary Table S5. Gene status of tumor cell lines. Supplementary Table S6. siRNAs used in this study. Supplementary Table S7. Antibody for immunoblotting used in this study. Supplementary Table S8. TaqMan® Gene Expression Assays used in this study. Supplementary Table S9. Primer used in this study.