Fig. 2

MiR155HG stimulated the ANXA2 expression by sponging endogenous miR-185-5p. a The binding site of MiR155HG and miR-185-5p was predicted by bioinformatics tools. b Expression levels of miR-185-5p in GBM tissues and adjacent normal brain tissues were analyzed by real-time PCR and normalized to U6. The correlation between MiR155HG and miR-185-5p in GBM tissues was applied with Pearson’s correlation coefficient (r = − 0.5970, P = 0.0021). c Luciferase assays was performed after transfection with miR-185-5p mimic and pGL3- miR155HG-wt or pGL3- miR155HG-mut into U87 cells as well as the internal control Renilla plasmid. Relative luciferase activity was analyzed after 48 h treatment. (*p < 0.05, **p < 0.01). d Amount of miR155HG bound to Ago2 or IgG measured by RT–qPCR after RIP assays with anti- IgG, anti-Ago2, anti-SNRNP70 and 10% input. e The binding site in 3’UTR of ANXA2 mRNA for miR-185-5p was predicted by bioinformatics tools. f Expression levels of ANXA2 in GBM tissues and adjacent normal brain tissues were analyzed by western blot and normalized to β-actin. The correlation between miR-185-5p and ANXA2 in GBM tissues was applied with Pearson’s correlation coefficient (r = − 0.4676, P = 0.0212). g Luciferase assays was performed after transfection with miR-185-5p mimic and pGL3- ANXA2-wt or pGL3- ANXA2-mut into U87 and GP1 cells as well as the internal control Renilla plasmid. Relative luciferase activity was analyzed after 48 h treatment. (*p < 0.05, **p < 0.01). h The protein expression levels of ANXA2 were analyzed by Western blotting after 48 h transfection in U87 cells with pcDNA3.1, pcDNA3.1-miR155HG wt, pcDNA3.1-miR155HG mut, miR-NC or different amount of miR-185-5p mimic, respectively