Fig. 1 | Scientific Reports

Fig. 1

From: Mechanism and role of H. pylori CagA-induced NLRP3 inflammasome in gastric cancer immune cell infiltration

Fig. 1

H. pylori infection promotes NLRP3 overexpression in gastric cancer. (A) Comparison and analysis results of the expression of each inflammasome between gastric cancer and normal tissues in the TCGA database by paired t-test. (B) Comparison and analysis results of the expression of each inflammasome between gastric cancer and normal tissues in the TCGA database by unpaired t-test. (C) The expression differences of NLRP3 between pan-cancer tissues and normal tissues shown by TIMER 2.0 data. (D) Heatmap of gene expression differences in H. pylori-infected positive and negative gastric cancer tissues from the TCGA database (top 50 genes). (E) Volcano plot of differentially expressed genes in gastric cancer tissues. (F) IHC detection results of NLRP3 expression in H. pylori-infected positive and negative gastric cancer tissues. (G) NLRP3 mRNA expression levels in H. pylori-infected positive and negative gastric cancer tissues. *P < 0.05, ** P < 0.01, *** P < 0.001; GC, gastric cancer; H. pylori( +), H.pylori-infected positive; H.pylori(-), H.pylori-infected negative.

Back to article page