Skip to main content
. 2009 Jan 8;23(3):412–421. doi: 10.1210/me.2008-0235

Figure 1.

Figure 1

ATO inhibits AR transcriptional activity. PC3 (A and D) LNCaP (B), or LAPC4 (C) cells were transfected with an ARE (D) or PSA (ARE containing)-luciferase reporter plasmid and AR cDNA expression vector (PC3 cells only). Cells were treated with either vehicle, 0.1 or 5 nm R1881 (an AR agonist), and either 0, 1, 2, or 5 μm ATO. Luciferase activity was determined 48 h after transfection. Means of triplicate samples are plotted± sem. E, TM4 cells were transfected with an ARE-luciferase reporter plasmid and treated with vehicle or 5 nm R1881 and 0 or 2 μm sodium arsenite. Luciferase activity was determined 48 h after transfection. F, LNCaP cells were treated with vehicle or 5 nm R1881 in the presence or absence of 2 μm ATO for 48 h. RNA was extracted and then reverse transcribed to cDNA. Real-time PCR was performed using Taqman probes for PSA mRNA and 18S mRNA (control). This experiment was performed three times under similar conditions. As, Arsenic; RLU, relative luciferase units.