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. 2021 Jun 4;13(11):2799. doi: 10.3390/cancers13112799

Figure 1.

Figure 1

The CBP/p300 interactome is dysregulated in luminal BC and ER is a major interaction partner for both CBP and p300. (A) Few CBP/p300 binding partners are essential for ER+ BC growth. Essential CBP/p300 binding partners (gene effect score ≤ −1) were identified in ER+ MCF-7 and HCC1419 BC cells. (B) ER shares many chromatin-binding sites with p300 and CBP in MCF-7 cells. The shared binding sites are represented as a percentage of shared chromatin-binding sites of the two factors noted in each bar with respect to total binding sites of p300, CBP and ER (data from Zwart et al. [52] and Yi et al. [21]). (C,F) The CBP/p300 interactome is dysregulated in luminal A (panel C) and B (panel F) BC. Differentially expressed (q-value < 0.05, |FC| ≥ 1.25) CBP/p300 binding partners are visualized via heatmap for luminal A (C) and B (F) BC subtypes. Data are from TCGA [57]. (D,G) CBP/p300 binding partners involved in ER signaling are upregulated in luminal BC. CBP/p300-binding partners that are upregulated (|FC| ≥ 1.25, q-value < 0.05) in luminal A (panel D) and B (panel G) BC were analyzed for Reactome Pathway enrichment. The top statistically enriched pathways are shown and pathways in red are involved in ER signaling. (E,H) Partners involved in ER signaling are among the top 14 most highly expressed CBP/p300 partners in luminal A (panel E) and B (panel H) BC (data from TCGA). The mean expression of each CBP/p300-binding partner was plotted and gene symbols in brown are members of the Estrogen Dependent Gene Expression Reactome Pathway.