摘要
肿瘤抑制基因p53是调节多种与细胞周期、凋亡、DNA修复等有关基因表达的转录因子。p53基因在大约30%的胶质瘤中发生突变,在胶质瘤的发生和发展中起重要作用。本文主要探讨野生型p53基因过表达对脑胶质瘤细胞系U251细胞生长抑制的机制。方法:通过p53腺病毒表达载体pAdCMV-p53及空载体pAdCMV-lacZ分别感染U251细胞系,RT-PCR及Westem blot方法检测转染效率;并通过MTT检测生长抑制率、流式细胞仪检测细胞周期及TUNEL检测分析细胞凋亡等指标观察p53基因对U251细胞生长的影响。结果:MOI为100时,野生型p53基因的过表达可引起U251细胞G_0、G_1期阻滞、诱导U251细胞凋亡以及引起U251细胞生长抑制。结论:p53基因可以通过细胞周期G_0、G_1期阻滞及诱导细胞凋亡抑制胶质瘤细胞系U251的生长。
BACKGROUND & OBJECTIVE:p53 is a transcription factor that regulates the expression of genes involved in the regulation of the cell cycle, apoptosis, DNA repair and angiogenesis. The mutation of p53 tumor suppressor gene has been found in 30% of gliomas, which plays a central role in both the genesis and progression of gliomas. This article will investigate the growth suppression effect of p53 gene on human glioma cell line U251. METHODS: U251 was infected with recombinant adenovirus encoding wild-type p53 gene. The expres-sion of exogenous p53 gene was confirmed by RT-PCR and Western blot analysis. The growth suppression effects of p53 were evaluated by MTT, flow cytometric analysis and TUNEL technique. RESULTS: Both of the G_1 arrest and apoptosis were detected after high efficiency expression of wild-type p53 gene in U251. CONCLUSIONS: The growth suppression effect mediated by the expression of exogenous p53 in U251 results mainly from apoptosis and G_1 arrest.
出处
《中国神经肿瘤杂志》
2004年第4期272-275,共4页
Chinese Journal of Neuro-Oncology
