电离辐射对人脑胶质瘤细胞NF-κB信号通路的作用及其机制

Ionizing radiation induces NF-κB activation in human glioblastoma cells

目的探讨电离辐射对人脑胶质瘤细胞核转录因子κB(NF-κB)通路的作用及机制。方法电离辐射(ionizing radiation,IR)诱导人胶质母细胞瘤T98G细胞(T98G细胞)DNA损伤;划痕、甲基噻唑蓝(MTT)比色实验及流式细胞仪检测细胞增殖及凋亡;Bay-11处理抑制NF-κB活性;双荧光素酶报告系统检测NF-κB的活性;免疫荧光检测p65的亚细胞定位。结果电离辐射不抑制T98G细胞增殖,不诱导其凋亡;抑制NF-κB的活性增强T98G细胞对电离辐射的敏感性;电离辐射能激活T98G细胞中NF-κB信号通路。结论电离辐射能激活T98G细胞的NF-κB信号通路。抑制NF-κB可增强T98G细胞对电离辐射的敏感性。

Objective The effects of ionizing radiation-induced nuclear factor-kappa B（NF-κB） activation in human glioblastoma cells are discussed. Methods Ionizing radiation （IR） was performed to induce DNA damage. Wound healing, methy thiazolyl tetrazolium （MTT） and annexin V and PI double-staining assays were used to detect cell migration, proliferation and apoptosis, respectively. Bay-11 treatment was performed to inhibit NF-KB activity. Dual-luciferase assays were performed to detect NF-κB activity. The nuclear translocation of p65 was detected by immunofluorescence. Results IR treatment had no significant effect on cell migration, proliferation or apoptosis in T98G cells. However, incubation with a NF-κB inhibitor Bayll attenuated migration and proliferation in 198G cells upon IR exposure. Conclusion IR-induced NF-κB activation contributes to radioresistance in human glioblastoma cells T98G.