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. 2014 Dec 22;34(4):502–516. doi: 10.15252/embj.201490306

Figure 5.

Figure 5

Antagonists display inhibitory efficacy on agonist-responsive ARBEs
  1. Heat map showing raw tags distribution over the four types of agonist-responsive ARBEs in LNCaP cells treated with vehicle, bicalutamide (10 μM), bicalutamide plus DHT (10 nM), enzalutamide (10 μM), or enzalutamide plus DHT (10 nM). The order of sequences in each type of ARBE is the same as the order of sequences shown in Fig2A.
  2. UCSC genome browser views of sequencing data at KLK3 locus under different conditions.
  3. Regular ChIP analysis of AR on KLK3 enhancer. LNCaP cells were treated with or without agonist and antagonist for 4 h. The data are presented as the fold enrichment over IgG (mean ± SD,n = 3).
  4. Quantitative RT-PCR was performed to assess KLK3 mRNA levels under agonist or antagonist treatments. The data are the mean of triplicates ± SD.
  5. Eight agonist-responsive ARBE reporter constructs used in Fig3B were transiently transfected into LNCaP cells. Cells were stimulated with vehicle, DHT (100 nM), bicalutamide (10 μM), bicalutamide plus DHT, enzalutamide (10 μM), or enzalutamide plus DHT for 16–24 h, and luciferase activities were measured. The results are presented as the mean ± SD of the quadruplicate transfections.