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Fig. 2 | Biomarker Research

Fig. 2

From: STAT3–mediated up-regulation of DAB2 via SRC-YAP1 signaling axis promotes Helicobacter pylori-driven gastric tumorigenesis

Fig. 2

H pylori infection upregulated DAB2 expression through STAT3. A GSEA based on gene expression analysis of GC in TCGA and Fudan database indicated that DAB2 has a significant correlation with JAK/STAT signaling in GC. NES, normalized enrichment score. B-C Western blot and qRT-PCR analysis of DAB2 in AGS and HGC27 cells following H pylori infection; *P < 0.05, **P < 0.01, ***P < 0.001. D-E Western blot and qRT-PCR analysis of DAB2 in AGS and HGC27 cells treated with STAT3 and IL6; **P < 0.01, ***P < 0.001. F Western blot and qRT-PCR data shows that DAB2 and p-STAT3 after H pylori infection and napabucasin treatment in AGS cells; *P < 0.05, **P < 0.01. G Western blot analysis shows DAB2 and p-STAT3 in gastric tissues of wildtype mice infected with PMSS1 H pylori for 2 weeks compared with noninfected mice. H qRT-PCR analysis of DAB2 in gastric tissues of wildtype mice infected with PMSS1 H pylori for 2 weeks. **P < 0.01. I IF analysis shows DAB2 and p-STAT3 in gastric tissues of mice infected with PMSS1 H pylori for 2 weeks compared with noninfected mice (magnification ×50, scale bar, 200 μm). Quantification of p-STAT3 is shown on the right panel; **P < 0.01. J IF data of DAB2 and p-STAT3 staining in uninfected and H pylori 26,695–infected organoids derived from normal human gastric tissues. Quantification of positive p-STAT3 cells was performed (magnification ×200, scale bar, 20 μm). Quantification of positive p-STAT3 cells was shown; **P < 0.01 (right panel)

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