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Fig. 2 | Journal of Experimental & Clinical Cancer Research

Fig. 2

From: The BRD4 inhibitor JQ1 augments the antitumor efficacy of abemaciclib in preclinical models of gastric carcinoma

Fig. 2

JQ1 is a promising candidate in combination with ABE. A Ranked synergy models of ABE and screened epigenetic drugs, including JQ1, tazemetostat, vorinostat, 5-azacitidine, SETDB1-TTD-IN-1 and UNC669. Synergy scores were labelled to the top of each model. B Dependency score of CDK4 and BRD4 for tumor cells across different cancer types. Score < 0 represents essential genes and Score < -1 represents super essential genes. C Transcriptional expression level of BRD4 between tumor and normal tissues in TCGA-STAD cohort. D Immunohistochemistry (IHC) staining of BRD4 in GC patients from The Human Protein Atlas. E CUT&Tag-seq binding enrichment of H3K27ac in AGS cells treated with DMSO or ABE. F Pie plot of the genomic distribution of H3K27ac peaks in ABE-treated AGS cells. G Gene tracks depicting H3K27ac signals at the BRD4 locus. The signal from ABE and DMSO was normalized at same level. H Western blotting images showing the protein level of BRD4 protein level after ABE treatment. GAPDH was used as a loading control. I Quantification of the protein level of BRD4 in AGS cells after ABE treatment for 24 h using ImageJ software. The data are presented as the mean ± SEM of three replicates. J Enrichment analysis of top1000 upregulated H3K27ac peaks in ABE-treated AGS cells. K Gene tracks depicting H3K27ac signals at the SMAD3, VCL, SNAI1 and RAC1 locus. The signals from ABE and DMSO were normalized at same level

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