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. Author manuscript; available in PMC: 2021 Aug 15.
Published in final edited form as: Cancer Res. 2020 Dec 21;81(4):820–833. doi: 10.1158/0008-5472.CAN-20-1417

Fig. 6:

Fig. 6:

BRD9 binds with BRD4 at AR-dependent genes. a Annotation of BRD9 and BRD4 ChIP-Seq peaks in LNCaP cells based on distance to gene coding regions in the hg19 genome. b Metagene analysis of BRD9 and BRD4 ChIP-Seq signal ± 5kb from center of BRD9 peaks (top) and BRD4 peaks (bottom). c (left)-Venn diagram of overlapping peaks from BRD9, BRD4, and AR (from [15]). ChIP-Seq in LNCaP cells. (right) Venn diagram of the overlap between the nearest gene defined for AR/BRD9/BRD4 shared peaks, and genes decreased with 48h of 10μM ENZA treatment [40]. d Genome browser tracks for BRD9 and BRD4 ChIP-Seq enrichment at the BMPR1B, KLK3, and TMPRSS2 loci. Peak sites from AR (GSM3223722) and BAF155 (GSM3223719) ChIP-Seq in LNCaP [15] depicted below. Regions analyzed with ChIP-qPCR are highlighted in boxes. e ChIP-qPCR of BRD9 and BRD4 enrichment at BMPR1B, KLK3, and TMPRSS2 enhancers after 24h DMSO or 10 μM I-BRD9 in LNCaP cells. f AR and BRD9 ChIP-qPCR for BMPR1B, KLK3 and TMPRSS2 sites during androgen stimulation with DMSO, 10 μM I-BRD9, and 1 μM JQ1 in LNCaP cells. g ChIP-qPCR of AR enrichment at BMPR1B, KLK3, and TMPRSS2 sites. Representative of two independent experiments with n=3 replicates. Error bars represent s.d. Statistical significance calculated using unpaired t-test. * p<0.05; ** p<0.01; *** p<0.001; **** p<0.0001.