CXCL12-CXCR4 axis mediates the effects of JMJD3 on the epithelial-mesenchymal transition and migration in glioma cells. U-251MG and U-87MG ATCC cells were ectopically expressing JMJD3 or CXCL12, respectively, or JMJD3 plus pretreatment with AMD3100. (A) mRNA expression levels of CXCL12, CXCR4, E-cadherin, N-cadherin and fibronectin in U-251MG (upper panel) and U-87MG ATCC (lower panel) cells. (B) Protein expression levels of JMJD3, E-cadherin, N-cadherin, CXCL12, CXCR4 and H3K27me3 were determined by western blotting in U-251MG and U-87MG ATCC cells. (C) Wound healing assay to evaluate the motility of the wild-type control, vector control, JMJD3 overexpression, CXCL12 overexpression and JMJD3 overexpression plus pretreatment with AMD3100 U-251MG and U-87MG ATCC cells. Magnification, ×10. (D) Statistical results for the interval distance of the wound healing assay. (E) Representative DAPI staining images and (F) quantification of fields in the Transwell assay for the wild-type control, vector control, JMJD3 overexpression, CXCL12 overexpression and JMJD3 overexpression and pretreatment with AMD3100 U-251MG and U-87MG ATCC cell groups. Scale bar, 200 µm. **P<0.01. ATCC, American Type Culture Collection; CXCL12, C-X-C motif chemokine ligand 12; CXCR4, C-X-C motif chemokine receptor 4; H3K27me3, histone H3 lysine 27 trimethyl; JMJD3, Jumonji domain-containing protein 3.