Figure 1.

Helicobacter pylori (H. pylori)-mediated niche environment aberrations promote the progression of gastric cancer. (A) The UMAP plot showing the cell clusters in intestinal metaplasia (IM) with and without H. pylori infection, including PMCs (pit mucous cells), T cells, fibroblasts, endothelial cells, GMCs (antral basal gland mucous cells), ECs (enteroendocrine cells), enterocytes, stem cells, PCs (proliferative cells), macrophages, B cells, epithelial cells, mast cells, and goblet cells. (B) The proportion of different cell types in H. pylori-infected and non-infected groups. (C) The dot plot showing the representative genes in the NF-κB signaling pathway and inflammatory cytokines in each cell type. (D) The volcano plot showing the up-regulated and down-regulated genes in PMCs. Significant differential expressed genes (DEGs) were defined as log fold change ≥1 or ≤−1 and adjusted P-value < 0.05 using the Wilcoxon rank-sum test. (E) The marker genes in “negative regulation of cell population proliferation” pathways with distinct expression patterns in the H. pylori-infected group versus the non-infected group. (F) The chord plot showing the signaling pathways among PMCs, GMCs, PCs, macrophages, fibroblasts, and T cells in the H. pylori uninfected and infected groups. (G) The ridge plot showing the difference in regulon activity among different cell subtypes. The regulon activity of FOXO1 had a distinct pattern in PMCs versus other cells. (H) The violin plot showing the difference in regulon activity of FOXO1 in PMCs with H. pylori infection versus the normal sample. ^∗∗∗∗P ≤ 0.0001.