作者: Che Liu , Defang Luo , Brent A. Reynolds , Geeta Meher , Alan R. Katritzky
关键词:
摘要: Human glioblastoma multiforme (GBM) is the most common primary brain tumor in adults. The poor prognosis and minimally successful treatments of GBM indicates a need to identify new therapeutic targets. In this study, we examined role CXCR3 glioma progression using GL261 murine model malignant glioma. Intracranial tumors express CXCL9 CXCL10 vivo. Glioma-bearing CXCR3-deficient mice had significantly shorter median survival time reduced numbers tumor-infiltrated natural killer T cells as compared with tumor-bearing wild-type (WT) mice. contrast, pharmacological antagonism NBI-74330 prolonged times both WT when vehicle-treated groups. treatment did not impact infiltration lymphocytes microglia. A small percentage were identified CXCR3+, which was similar expression several grade IV human cell lines (A172, T98G, U87, U118 U138). When cultured gliomaspheres (GS), increased expression; also found GBM-derived GS. Additionally, isoform expressed by all lines, whereas CXCR3-B detected T98G-, U118- U138-GS cells. or induced vitro growth GL261- U87-GS well inhibited loss effect antagonized NBI-74330. results suggest that exerts direct anti-glioma receptor may be potential target for treating GBM.