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. Author manuscript; available in PMC: 2020 Oct 29.
Published in final edited form as: Oncogene. 2020 Apr 29;39(22):4465–4474. doi: 10.1038/s41388-020-1304-6

Figure 4.

Figure 4.

Effect of SMOX activity on β-catenin activation in human-derived gastric organoids. (A) Polyamine levels measured by mass spectrometry in monolayers of human gastric organoids pre-treated with SLH150–54 (100 μM) for 2 h and then infected with H. pylori PMSS1 for 16 h. (B) TCF/LEF reporter assay in human GECs pre-treated with with SLH150–54 and then infected with H. pylori PMSS1 for 6 h. (C) AXIN2 mRNA expression in human GECs pre-treated with SLH 150–54 and/or infected for 3 h with H. pylori. (D) Immunofluorescence staining for β-catenin was performed on human organoid GEC monolayers pre-treated with SLH150–54 and supplemented or not with spermidine (10 μM), then infected with H. pylori PMSS1 for 16 h; representative image from three experiments, performed with two human organoid lines. The merged images are shown, β-catenin is green, and nuclei are blue; scale bar, 100 μm. (E) The fluorescence of images shown in (D) was quantified by measuring the translocation of β-catenin to the cytoplasm and nucleus using ImageJ. Mean ± SEM of three experiments with two organoid lines. **P<0.01, ***P<0.001 compared to control cells; §§§ P<0.001 versus H. pylori-infected cells; # P<0.05 versus H. pylori-infected cells pre-treated with SLH150–54.