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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 possible mechanism of IL-24 inhibiting human glioma cell proliferation. Methods: Human glioma cell line U251 was infected with adenovirus mediated Ad-IL-24 (Ad.IL-24) and adenovirus empty vector. The infection efficiency of adenovirus was observed by fluorescence microscopy. The expression of IL-24 The effect of IL-24 on the proliferation of U251 cells was detected by MTT assay and flow cytometry. The expressions of NGF, tyrosine kinase A (TrkA) Expression level, and analyze its correlation. Results: Ad-IL-24 and adenovirus empty vector transfected U251, RT-PCR results showed that Ad.IL-24 group of high expression of electrophoresis bands, adenovirus empty vector group did not appear electrophoresis bands; MTT results The results showed that Ad.IL-24 significantly inhibited the proliferation of U251 cells, and flow cytometry cell cycle assay showed that the G2 / M phase of Ad.IL-24 treatment group was significantly prolonged compared with the control group, Western blot results showed that over-expression of IL-24 U251 cells NGF and TrkA expression decreased. Conclusion: IL-24 may inhibit the proliferation of tumor cells by decreasing the expression of TrkA and NGF in the cells.