Fig. 3

KLF4 bound to the promoter of BIK. a Schematic illustration of pGL3-based reported constructs were used in luciferase assays to examine the transcriptional activity of BIK. b Parts of the promoter of BIK, named P1, P2 and P3, were individually transfected into PC3 cells with or without 20 μM cisplatin treatment. Luciferase activity was measured. Data represent the mean ± SD of three independent experiments. **p < 0.01, *** p < 0.001 vs. control. c The promoter of BIK, named P1, was transfected into PC3 and DU145 cells with or without KLF4 KO and then the cells were treated with 20 μM cisplatin at the indicated times. Luciferase activity was measured. Data represent the mean ± SD of three independent experiments. ***p < 0.001 vs. control. d The potential KLF4 binding sites were inspected by JASPAR. Schematic illustration of KLF4 wild type binding site (BS) and the matching mutant (BSM) that were used in luciferase assays. e-f The wild type promoter (BS) or the matching mutant (BSM) were individually transfected into PC3 cells with or without KLF4 knockout and the cells then were treated with 20 μM cisplatin for the indicated times. Luciferase activity was measured. Data represent the mean ± SD of three independent experiments. *** p < 0.001 vs. control. g-h ChIP analysis showing the binding of KLF4 to the promoter of BIK in KLF4 WT or KO PC3 cells in response to 20 μM cisplatin treatment. An isotype-matched IgG was used as a negative control