摘要
目的:探讨IL-24抑制人脑胶质瘤细胞增殖的可能机制。方法:用腺病毒介导的IL-24(Ad.IL-24)及腺病毒空载体感染人脑胶质瘤细胞U251,通过荧光显微镜观察腺病毒的感染效率,RT-PCR法检测IL-24的转录水平;用MTT法、流式细胞仪检测IL-24对U251细胞增殖的影响;用蛋白质印迹方法检测神经生长因子(NGF)、酪氨酸激酶受体A(tyrosine kinase A,TrkA)的表达水平,并分析其相关性。结果:Ad.IL-24及腺病毒空载体转染U251后,RT-PCR结果显示Ad.IL-24组出现高表达电泳条带,而腺病毒空载体组则未出现电泳条带;MTT结果显示Ad.IL-24明显抑制了U251细胞的增殖,且流式细胞仪细胞周期检测发现Ad.IL-24处理组较对照组G2/M期明显延长,蛋白质印迹结果显示过表达IL-24的U251细胞中NGF及TrkA表达降低。结论:IL-24可能通过减少细胞中TrkA和NGF的表达来抑制肿瘤细胞的增殖。
Objective: To investigate the effect of Ad-IL-24 on proliferation of glioma cells and explore its probable mechanism.Methods: U251 were infected with Ad-IL-24;Microscope was used for observing the infection efficiency,and RT-PCR for examining the transcription level of IL-24,MTT and FACS for investigating the effect of IL-24 on the proliferation of U251,Western Blot for detecting expression of nerve growth factor(NGF) and tyrosine kinase A(TrkA) and analyzing association between them.Results: All of the methods revealed that IL-24 expressed well in U251 cells and inhibited the proliferation of U251 significantly.G2/M phase was prolonged by IL-24 also.Moreover,overexpression of IL-24 result in decreasion of NGF and TrKA.Conclusion: IL-24 mediated inhibition of the proliferation of human glioma cells was resulted from decreasing expression of NGF and TrKA.
出处
《江苏大学学报(医学版)》
CAS
2010年第3期203-206,共4页
Journal of Jiangsu University:Medicine Edition
基金
江苏省高校自然科学基金资助项目(07KJB310018)
江苏大学大学生科研项目(07A126
08A226)