Fig. 6

KLF4 binds to the promoter of ITGB4. a Schematic illustration of pGL3-based reporter constructs were used in luciferase assays to examine the transcriptional activity of ITGB4. b-c Parts of the promoter of ITGB4, named P1, P2, and P3, were individually transfected into LN229 and U251 cells with or without KLF4 overexpression. Luciferase activity was measured. Data represent the mean ± SD of three independent experiments. *** p < 0.001 vs. control. d-e Parts of the promoter of ITGB4, named P1, P2, and P3, were individually transfected into LN229 and U251 cells with or without KLF4 knockdown. Luciferase activity was measured. Data represent the mean ± SD of three independent experiments. ** p < 0.01, *** p < 0.001 vs. control. f The potential KLF4 binding site was inspected by JASPAR. Schematic illustration of KLF4 wild type binding site (BS) and the matching mutant (BSM) that were used in luciferase assays. g-h The wild type promoter (BS) or the matching mutant (BSM) were individually transfected into LN229 and U251 cells with or without KLF4 overexpression. Luciferase activity was measured. Data represent the mean ± SD of three independent experiments. ** p < 0.01 vs. control. i-j ChIP analysis showing the binding of KLF4 to the promoter of ITGB4 in LN229 cells with or without KLF4 overexpression or knockdown. An isotype-matched IgG was used as a negative control