中文摘要：

目的观察磷脂酰肌醇-3-激酶（PI3K）的调节亚单位——p55PIKN端24个氨基酸抑制肝癌细胞增殖的作用。方法以含有p55PIK-N端24个氨基酸（N24）的腺病毒载体Ad-N24-GFP及对照病毒Ad-GFP,感染肝癌HepG2细胞,流式细胞仪检测细胞周期进程,应用BrdU掺入的方法检测其对细胞DNA合成的影响,Western blot分析细胞内高表达N24多肽后相关蛋白的表达水平。结果N24能有效阻滞HepG2细胞周期进程于G0/G1期,S期和G2/M期细胞减少,Ad-N24-GFP组各期细胞分布为：G0/G1期（56.3±3.0）%,S期（30.1±2.9）%,G2/M期（13.6±4.1）%,而对照组腺病毒各期细胞分布为：G0/G1期（40.6±2.1）%,S期（42.7±3.3）%,G2/M期（16.7±2.8）%;BrdU阳性细胞比例显示：Ad-N24-GFP组R2为（31.8±5.2）%,Ad-GFP组R2为（48.5±3.7）%,提示N24能有效抑制HepG2细胞的DNA合成;Western blot检测显示高表达N24对细胞内的AKT磷酸化水平没有显著影响。结论在HepG2细胞中过表达N24能有效阻滞肝癌细胞周期进程,抑制细胞DNA合成。p55PIK为肿瘤的基因治疗提供了一个新的分子靶点。

英文摘要：

Objective To investigate the anti-proliferation function of n-terminal 24 amino acids of p55PIK（N24） in hepatic cancer cells.Methods Adenovirus vectors loading N24P55PIK over-expressed N24 polypeptides in HepG2 cell lines.Cell cycle progression was analyzed by flow cytometry,while BrdU incorporation technology was performed to measure DNA synthesis.Western blot was used to detect the expression level of phosphorylated AKT.Results N24 blocked cell cycle at G0/G1 phase,and the cells in S,and G2/M phases were decreased.In Ad-N24-GFP group,the percentage of cells in G0/G1 phase was（56.3±3.0）%,（30.1±2.9）% in S phase,and（13.6±4.1）% in G2/M.In control group,the percentage of cells in G0/G1 phase was（40.6±2.1）%,（42.7±3.3）% in S phase,and（16.7±2.8）% in G2/M phase.The proportion of BrdU positive cells in Ad-N24-GFP group was R2：（31.8±5.2）%,and that in Ad-GFP group was R2：（48.5±3.7）%,suggesting N24 could inhib DNA synthesis of HepG2 cells effectively.Western blot revealed that N24 over-expression had no significant effects on phosphorylation state of AKT.Conclusion The N24 over-expression in HepG2 cells could effectively inhibit the DNA synthesis and arrest cell cycle progression.P55PIK provides a new molecular target point for gene therapy of cancer.