Fig. 6

XPR1 promote the malignant phenotype of GSCs via IL6/JAK2/STAT3 signaling axis. a, b CGGA and TCGA datasets showed that the expression of XPR1 was positively related to enrichment of IL6-mediate JAK2/STAT3 signaling. c–h qRT-PCR (c), ELISA (d), and western blotting (e–h) revealed that XPR1 could alter the expression of IL6 via JAK2/STAT3 axis in GSCs. i–n MTS (i, j), Edu (k, m) and transwell (l, n) assays indicated that IL6 could reverse the cell viabilities, proliferation abilities, and invasion capabilities repressed by XPR1 knockdown in GSC27, whereas anti-IL6 could reverse the cell viabilities, proliferation abilities, and invasion capabilities promoted by XPR1 overexpression in GSC23; o–r The neurosphere formation (o, p) and limiting dilution assays (q, r) demonstrated that IL6 could reverse the size of neurosphere repressed by XPR1 knockdown, whereas anti-IL6 could reverse the neurosphere-forming capacity promoted by XPR1 overexpression. Data represent mean ± SD (three independent experiments). *p < 0.05; **p < 0.01; ***p < 0.001