Fig. 5. ABL2 directly targets miR-16-5p and its expression increases within GC tissues, which is related to GC development and dismal survival.

A Public databases predicted that ABL2 may be miR-16-5p downstream protein. B and C Western blotting revealed that miR-16-5p mimics downregulated the ABL2 expression and miR-16-5p inhibitor upregulated the expression of ABL2. D and F Western blotting and immunofluorescence revealed that overexpression of circPGD in BGC-823 cells could increased the ABL2 protein level (scale bars = 25 μm). E and G circPGD silencing within MGC-803 cells decreased the ABL2 protein expression. H Luciferase reporter assay showed that there are binding sites in miR-16-5p and ABL2. I MiR-16-5p mimics could reduce ABL2 level induced by the circPGD plasmid. J MiR-16-5p inhibitor can enhance ABL2 expression, which was inhibited by the circPGD siRNA. K ABL2 mRNA expression within healthy samples (n = 95) as well as GC samples (n = 99) with ONCOMINE. L ABL2 mRNA levels within 50 GC tissues as well as 50 corresponding non-tumor samples detected through qRT-PCR revealed that it was upregulated in tumor tissues. M ABL2 level showed negative correlation with miR-16-5p level. N Immunohistochemistry was carried out for detecting ABL2 levels within GC samples compared with corresponding non-tumorous samples (original magnification, ×200). O Detection of the ABL2 expression levels within GES-1 cells as well as six GC cell lines by western blotting. P Influence of the ABL2 expression level on OS and PFS in GC cases was examined by the Kaplan–Meier Plotter. Q The ABL2 level was positively correlated with circPGD expression. *p < 0.05, **p < 0.01, ***p < 0.001.