Fig. 4

The miR-148/152 family genes may be involved in the progression of gastric cancer by targeting ITGA5. A Prediction of miRNA for ITGA5 regulation. The four ovals in the figure represent the prediction results of ITGA5-regulated miRNA in the four databases respectively, and the middle part represents the intersection of the prediction results of the four databases. B The expression of miR-148a, miR-148b, and miR-152 in 52 pairs of gastric cancer and adjacent normal tissue samples (n = 52) examined by RT-qPCR. *p < 0.05 and **p < 0.01 compared with adjacent normal tissue samples. C Kaplan–Meier curve analysis of the correlation of the overall survival of 52 patients with gastric cancer with miR-148a expression. D Kaplan–Meier curve analysis of the correlation of the overall survival of 52 gastric cancer patients with miR-148b expression. E Kaplan–Meier curve analysis of the correlation of the overall survival of 52 patients with gastric cancer with miR-152 expression. F Pearson analyzed the correlation between miR-148/152 family genes and ITAG5 genes in clinical cancer samples. G The expression of miR-148a, miR-148b, and miR-152 in gastric cancer cell lines (MKN45, AGS, KATO-III, NCI-N87, and SNU-1) and normal immortalized gastric mucosal cells GES-1 examined by RT-qPCR. *p < 0.05 compared with GES-1 cells. H The expression of miR-148/152 family genes in CD44⁺EpCAM⁺ cells and CD44⁻EpCAM⁻ was detected by RT-qPCR. I TargetScan software predicted the potential target-binding sites of miR-148/152 and ITGA5. J Binding of miR-148a, miR-148b, and miR-152 to ITGA5 confirmed by dual-luciferase reporter assay. K Western blots and quantification of ITGA5 protein in AGS cells treated with miR-148a mimic, miR-148b mimic, and miR-152 mimic, normalized to GAPDH. *p < 0.05 compared with GSE-1 cells, CD44⁻EpCAM⁻ or mimic-NC. The cell experiment was run in triplicate independently