Fig. 5

CircGNB1 mediated the malignant phenotype of GSCs by acting as ceRNA of miR-515-5p and miR-582-3p to regulate XPR1 expression. a–d qPCR assays showed miR-515-5p/miR-582-3p inhibitor could reverse the expression of XPR1 reduced by circGNB1 knockdown, while miR-515-5p/miR-582-3p mimic could subside the expression of XPR1 promoted by circGNB1 overexpression in GSCs. e–h Western blotting revealed the effects of miR-515-5p/miR-582-3p inhibitor (or mimic) on XPR1 protein expression. i, j MTS assays showed XPR1 knockdown reversed the cell viabilities promoted by circGNB1 overexpression. k, l Edu assays showed that XPR1 knockdown reversed the positive rates of GSC23 and U251 caused by circGNB1 overexpression. m, n The transwell assays revealed that XPR1 knockdown could reverse the invasion capabilities enhanced by circGNB1 overexpression. o, p The neurosphere formation assays demonstrated that XPR1 knockdown could reverse the size of neurosphere promoted by circGNB1 overexpression. q, r The limiting dilution assays showed that XPR1 knockdown affected the neurosphere-forming capacity of GSCs with circGNB1 overexpression. Data represent mean ± SD (three independent experiments). *p < 0.05; **p < 0.01; ***p < 0.001