Fig. 4: MYC overexpression alters the AR cistrome. | Nature Communications

Fig. 4: MYC overexpression alters the AR cistrome.

From: MYC drives aggressive prostate cancer by disrupting transcriptional pause release at androgen receptor targets

Fig. 4

a AR ChIP-seq identifies an androgen response element (ARE) as the top AR binding motif in WT and MYC-transformed VP (VP; n = 2 pools of biological replicates (n = 8–13) per genotype). b Unsupervised pairwise correlation of the murine AR cistrome from all specimens (VP; n = 2 pools of biological replicates (n = 8–13) per genotype). c MYC overexpression expands the AR cistrome as demonstrated by the heatmaps indicating AR binding intensity across 4 kb intervals (VP; n = 2 pools of biological replicates (n = 8–13) per genotype). d Motif analysis of MYC-associated AR gained sites reveal forkhead response element (FHRE) and androgen response element (ARE; VP; n = 2 pools of biological replicates (n = 8–13) per genotype). e, f AR gained sites are characterized by increased FOXA1 binding (e) and H3K27ac mark (f) in MYC-transformed VP (VP; n = 2 pools of biological replicates (n = 8–13) per genotype). g Integration of the 1695 AR bindings sites gained in MYC tumors with luminal single cell transcriptome grouped by k-means clustering (n = 3 clusters). h GSEA analysis (Hallmark) revealed an enforced MYC transcriptional program (Cluster 1) and a diminished androgen response (Cluster 2) associated to MYC-dependent AR gained binding sites (Source data are provided as a Source Data file).

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