In conclusion, our findings suggest that downregulation of the CCL2/CCR2 and CXCL10/CXCR3 axes via inhibition of the NF-κB pathway in the tumor and the tumor microenvironment might have contributed to the antitumor effects of celecoxib observed in the mouse glioma model. This evidence concerns the gene CXCL10 and central nervous system cancer.