<p>In all experiments, AGS cells were infected or not (NI) with <i>cagPAI+ H. pylori</i> (WT) at MOI 100 bacteria/cells for 24 h. (A) Activities of SV40 promoter (pGL3-p), or <i>miR-200b-200a-429</i> promoter wild type (pGL3-prom200b) or mutated on the NF-κB site (pGL3-prom200b mut); bars represent mean ± SD of relative luciferase activities of each promoter reporter normalized to that of NI pGL3-p transfected cells (n = 3; ** p<0.01). (B) NF-κB activation upon infection (WT) in cells transfected either with pEGFP or with pEGFP-IκB. Bars represent mean ± SD of relative NF-κB reporter luciferase activity compared to NI pEGFP-transfected cells (n = 3; *p<0.05). (C) Cell morphology observed by phase contrast microscopy, in the same conditions. Bar, 20 µm. (D) RT-qPCR data of ZEB1 and pri-miR-200b-200a-429 in pEGFP- or pEGFP-IκB-transfected cells. Bars indicate mean ± SD of RNA expression normalized to HPRT1 and compared to NI (n = 3, * p<0.05, *** p<0.001). (E) <i>MiR-200b-200a-429</i> promoter activities measured as in (A) in cells transfected either with pEGFP or with pEGFP-IκB. (F) Chromatin immunoprecipitation assays using anti-NF-κB antibody on the promoters of miR-200b (prom200b), IL-8 (promIL-8) or ZEB1 (promZEB1). Bars represent NF-κB enrichment on a given promoter in either uninfected or infected cells, calculated as the following ratio: 2<sup>−ΔCt IPNF-κB</sup>/2<sup>−ΔCt controlIP</sup>, with ΔCt = Ct IP (with NF-κB antibody or without (control)) – Ct input (input corresponds to chromatin before immunoprecipitation).</p
