Fig. 1

CMTM3 expression increases during H. pylori infection. a CMTM3 expression level in the gastric mucosa from the same patient before and after H. pylori infection (n = 11) were investigated by immunohistochemistry of CMTM3. b Graph showing the average quantification of CMTM3-positive cells in at least 6 random fields of one patient. Data are expressed as means ± SEM. c Establishment of the C57BL/6 mouse model of H. pylori infection. d&e H. pylori colonization was identified by H. pylori immunohistochemical staining (d) and 16S rRNA qRT-PCR (e). f, g The gating strategy for the percentage of CMTM3-positive cells in mice gastric tissue (f). EPCAM is a maker of gastric mucosa epithelial. Total cells (1 × 10⁶) were counted for analysis. The percentage of CMTM3-positive cells in the Brucella broth (negative control, NC) and PMSS1 groups was compared (g). h–k CMTM3 expressions in GES-1 and AGS cells, treated with H. pylori, were detected by qRT-PCR (h, i) and western blotting (j, k). β-Actin was used as a loading control. Data is representative of three independent experiments and presented as the mean ± SEM. l Luciferase assay of GES-1 transfected with control (pGL3-Basic) or pGL3-Basic-CMTM3-promotor plasmid. Renilla vector was used as an internal control plasmid. The relative luciferase activity was calculated as Firefly/Renilla ratio. Data is representative of three independent experiments and presented as the mean ± SEM. *p < 0.05, **p < 0.01