Fig. 4

SULT2B1 deletion suppressed PI3K/AKT signaling in GES-1 cells and contributed to transformation upon 3-MCA induction. a, b The GES-1 and SULT2B1^−/− GES-1 cells were stimulated with IGF-1 (100 ng/mL, a) or EGF (100 ng/mL, b) for 5, 15, 30, 60, or 180 min. The phosphorylation levels of AKT were detected by Western blotting. The p-AKT/t-AKT ratios are plotted. c GES-1 and SULT2B1^−/− GES-1 cells were stimulated with IGF-1 (100 ng/mL) or EGF (100 ng/mL) for 8 h. The mRNA levels of the genes involved in gastric epithelial function were measured by qRT-PCR. d Immunofluorescent staining of claudin-1 [36] in GES-1 and SULT2B1^−/− GES-1 cells. The nuclei were revealed by DAPI staining (blue). e Wound healing assay of GES-1, SULT2B1^−/− GES-1 and SULT2B1^−/− GES-1 cells transfected with Ad-SULT2B1b. f GES-1 and SULT2B1^−/− GES-1 cells were treated with 3-MCA (2 μg/mL) for 14 days. 3-MCA was added into the medium every 2–3 days. The cell morphology is presented. g The mRNA levels of pro- and anticancerous genes were detected by qRT-PCR in GES-1 and SULT2B1^−/− GES-1 cells in the absence or presence of 3-MCA treatment for 14 days. * P < 0.05, ** P < 0.01