Fig. 2 | Scientific Reports

Fig. 2

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

Fig. 2

Analysis of differential miRNAs related to NLRP3 expression caused by H. pylori infection in gastric cancer and the expression level of miRNA 1290. (A) Co-culture of H. pylori and AGS. (B) Co-culture with CagA-positive H. pylori leads to the expression of CagA in AGS and GES-1. (C, D) Fluorescent protein expression in stable cell lines transfected with plasmids and cell morphology under bright-field illumination (E). (F) Western blot verification of CagA overexpression in plasmid-transfected cells. (G, H) Flow cytometry detection images and bar charts of apoptosis data. Bar charts of pyroptosis’s ROS (I), cytokines IL-1β (J), and IL-18 (K) detection data. (L) Volcano plot of differentially expressed miRNAs in gastric cancer. (M) Differential expression analysis of miRNA-1290 in gastric cancer and normal tissues. NLRP3 mRNA expression (N), NLRP3 protein levels (O) and miRNA-1290 levels (P) in AGS cells after CagA overexpression. (Q) Schematic diagram of the binding sites between miRNA-1290 and the 3’ UTR of NKD1. (R, S) Western blot verification and protein grayscale bar charts of NKD1 protein expression in AGS lines transfected with miRNA-1290 or inhibitors. (T) Bar chart of relative luciferase activity detection in each group of cells in the luciferase assay.

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