LRP16影响电离辐射诱导的NF-κB活性

LRP16 Affects Ionizing Radiation-Induced NF-κB Activity

目的:研究LRP16在电离辐射激活核转录因子NF-κB信号转导通路中的作用。方法:在HeLa细胞中,分别运用双萤光素酶分析和Western印迹检测LRP16对κB-Luc报告基因及NF-κB下游靶基因表达的影响。结果:双萤光素酶实验证实LRP16过表达促进电离辐射诱导的κB-Luc活性,而抑制LRP16则降低电离辐射诱导的κB-Luc活性;Western印迹结果显示,LRP16过表达促进电离辐射诱导NF-κB的下游抗凋亡基因XIAP的表达,与之相对应的是,抑制LRP16降低电离辐射诱导NF-κB下游抗凋亡基因XIAP的表达。结论:LRP16可以调节电离辐射诱导NF-κB的转录活性,并且调控NF-κB下游抗凋亡基因XIAP的表达,为进一步阐明电离辐射激活NF-κB转录活性的分子机制奠定了基础。

Objective： To study the role of LRP16 in the signal transduction pathways of ionizing radiation（IR）-induced nuclear factor-κB（NF-κB） activation.Methods： The effects of LRP16 on NF-κB response reporter（3×κB-Luc） and the down streaming target gene XIAP of NF-κB were measured by dual-luciferase report assay system and Western blotting respectively in HeLa cells.Results： The dual-luciferase report assay system showed that LRP16 overexpression increased the IR-induced relative luciferase activities of NF-κB response reporter and the inhibition of LRP16 expression decreased the IR-induced relative luciferase activities of NF-κB response reporter.Western blot also demonstrated that LRP16 overexpression strengthened the expression of the anti-apoptotic gene XIAP induced by NF-κB and the inhibition of LRP16 expression weakened the expression of the anti-apoptotic gene XIAP induced by NF-κB.Conclusion： LRP16 can enhance NF-κB transcriptional activity induced by IR and affect the expression of NF-κB-targeting anti-apoptotic gene XIAP induced by IR,which may provide a foundation for studying the molecular mechanism of IR-induced NF-κB transcriptional activation.