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. 2016 Jun 6;8(5):7489–7501. doi: 10.18632/oncotarget.9841

Figure 4. AHR physiologically regulates HDAC8 expression in normal mouse hepatocytes.

Figure 4

a, p < 0.001. A. The HDAC8 promoter with the −108 to −125 bp deletion abolished the promoter binding activity of AHR. B. Chromatin HDAC8 promoter binding activity showed an AHR-dependent increase in hepatoma cells. The HDAC8 promoter binding activity of the AHR complex in hepatoma cells determined with ChIP in vivo. C. Forced HDAC8 downregulated RB1 expression. D. Forced HDAC8 expression in hepatoma cells enhanced the chromatin binding activity of HDAC8 on the RB1 promoter. E. HDAC8 expression in hepatocytes was abrogated in AhR-null mice. F. The ablation of HDAC8 expression in hepatocytes showed involvement of AHR-dependent regulation. G. The hepatoma cells (SK-Hep1) transfected with HDAC8 showed to downregulate the enhancement on tumor suppressors, p53 and RB1, expression induced by cells transfected with AHR shRNAi.