H. pylori induces STAT3 nuclear translocation and transcriptional activation in a CagA-dependent manner. H. pylori induces STAT3 nuclear translocation and transcriptional activation in a CagA-dependent manner. A-C, HEp-2 cells were treated with culture media (A), IL-6 for 30 min (B), or infected with H. pylori strain 7.13 (C) for 4 h. Fixed cells were stained with anti-STAT3 and donkey anti-mouse Cy3 conjugated secondary antibodies. Confocal images were taken of representative cells for each treatment. D, whole nuclei of uninfected, IL-6–treated, and H. pylori–infected STAT3-GFP transfected cells were bleached, and the percentage recovery of fluorescence was measured relative to the initial values. Six cells for each group were analyzed. *, P < 0. 05, using the Student's t test (n = 4). HEp-2 cells were transfected with luciferase reporter constructs containing three repeat STAT3 DNA binding domains, p950m4, or control pSTAT3 plasmids. Transfected cells were treated with IL-6 or infected with H. pylori strain 60190 for 48 h, and luciferase activity was measured and normalized against Renilla luciferase activity. *, P < 0.05, using the Student's t test (n = 3). Dana M. Bronte-Tinkew et al. Cancer Res 2009;69:632-639 ©2009 by American Association for Cancer Research