Fig. 8

STAT3 transcriptionally suppresses miR-26b-5p. A MGC803 and HGC27 cells were treated with IL-6 at the concentration of 50 mg/ml for indicated times, and the expression of miR-26b-5p was detected by qRT-PCR. MGC803 B and HGC27 cells C were transfected with STAT3 siRNAs, and the expression of STAT3 and miR-26b-5p was examined using qRT-PCR. D MGC803 and HGC27 cells were transfected with STAT3 siRNAs or siNC and then treated with IL-6 (50 mg/ml). The expression of miR-26b-5p was detected by qRT-PCR. E HEK-293 T cells were co-transfected with pGL3-luciferase promoter plasmid containing the whole miR-26b-5p promoter region or pGL3-luciferase basic plasmid and STAT3 overexpression plasmids or control. The relative luciferase activities were determined 48 h after transfection. F The schematic model of miR-26b-5p-mediated GC proliferation. IL-6 induced by H.pylori infection activates STAT3 which directly suppresses miR-26b-5p expression, resulting in the upregulation of miR-26b-5p’s targets, PDE4B and CDK8. The increase of PDE4B and CDK8 causes GC proliferation through STAT3 signaling. Quantitative data are shown as the mean ± SD of three independent experiments. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001