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机构地区:[1]广州医学院病理生理学教研室,广东广州510182
出 处:《中国病理生理杂志》2013年第3期418-424,共7页Chinese Journal of Pathophysiology
基 金:国家自然科学基金资助项目(No.81101680);广州医学院青年基金资助项目(No.2010C11)
摘 要:目的:观察Bmi-1对人胶质瘤SNB19细胞生长恶化的影响。方法:体外培养人胶质瘤SNB19细胞,建立稳定表达Bmi-1和抑制Bmi-1表达的细胞系及空载体对照组细胞系。通过MTT、体外小室侵袭试验和血管内皮细胞成管试验检测胶质瘤细胞生长、侵袭运动和血管增生的能力。通过双萤光素酶信号报告系统和细胞免疫荧光染色检测NF-κB的活化程度。通过实时荧光定量PCR检测NF-κB下游基因表达水平。结果:Bmi-1体外增强胶质瘤细胞生长、侵袭运动和血管增生能力。高表达Bmi-1的细胞NF-κB信号通路被活化,而抑制NF-κB的活性能够抑制Bmi-1对胶质瘤细胞生长、侵袭和血管增生相关的促进作用。高表达Bmi-1的细胞其NF-κB下游与细胞生长、侵袭运动及血管增生相关的基因的表达被上调。结论:Bmi-1在人胶质瘤SNB19细胞生长过程中起到重要促进作用,其作用机制可能与活化NF-κB进而增强相关基因的表达有关。AIM: To study the effects of Bmi-1 on the progression of human glioma SNB19 cells. METH- ODS: Human glioma SNB19 cells stably overexpressing Bmi-1 were established, and Bmi-1 was knocked down using RNA interference (RNAi) methods. The proliferation, invasion and angiogenesis of SNB19 cells were detected by MIT, Tran- swell assay and tube formation. The activity of NF-KB was detected by dual-luciferase report assay and immunofluorescence cell staining. The NF-KB downstream gene expression was detected by real-time PCR. RESULTS: Bmi-1 dramatically in- creased the proliferation, invasiveness and angiogenesis of SNB19 cells. NF-κB transcriptional activity and NF-κB down- stream gene expression were significantly increased in the glioma cells which overexpressed Bmi-1. The proliferation, inva- sion and angiogenesis abilities of Bmi-l-overexpressing cells were dependent on the activity of NF-KB. CONCLUSION: Bmi-1 may play an important role in the development of human glioma SNB19 ceils, which might be correlated with NF-κB pathway activation and the relevant gene expression.
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