Helicobacter pylori promote gastric cancer cells invasion through a NF-kB and COX-2-mediated pathway

Figure 4 A: Transactivation of COX-2 promoter by NF-κB. MKN-45 cells were transiently transfected with full-length COX-2 promoter (Black bar), or mutated COX-2 construct, phPES2 (KBM), where the putative NF-κB binding domain was mutated (open bar), in the presence of p65, p50, or control vector (pMT2) plasmid. Luciferase and β-galactosidase activities were performed 48 h after transfection. (n = 4, P<0.05); B: Binding of nuclear NF-κB to COX-2 promoter DNA in MKN-45 cells. Nuclear protein was extracted from cells cultured in the absence (lane 2), or presence (lane 3) of H pylori. The protein-DNA interaction bands were shown as (→). Lane 1 showed free probe only.