本研究利用 RNAi 和蛋白点突变技术构建 E2F-1缺陷和 E2F-1 不同结构域功能缺陷的肝癌细胞，探讨蛋白 E2F-1 在 GL-V9 诱导肝癌细胞凋亡过程中的作用，观察在 GL-V9 处理的肝癌细胞中，蛋白 E2F-1 表达和后修饰状态的改变；通过考察这些 E2F-1 的变化对 DNA 损伤check point 蛋白、p73 及其下游促凋亡蛋白、内质网应激反应蛋白的表达的影响，将 ROS、内质网应激和凋亡蛋白等通过 E2F-1 整合成一个机整体，阐明 GL-V9 诱导细胞凋亡的机制；同时从 GL-V9 对 E2F-1 翻译后修饰方面开展研究，深入探讨 ER 应激激活和胞内 ROS 升高激活E2F-1的因素和其后修饰的类型，不仅可揭示影响 E2F-1 凋亡机制走向的因素和翻译后修饰类型在细胞凋亡中的作用，为开发以E2F-1为靶点的新型抗肿瘤药物提供新思路。

GL-V9 induces apoptosis of liver cancer cells through endoplasmic reticulum (ER) stress and E2F-1 expression by reactive oxygen species (ROS) increasing in cells. But it is unclear how E2F-1 is regulated in theGL-V9-mediated ER stress. When DNA damage emerges, E2F-1 is activated and can induce cells apoptosis through the p53-dependent and p53-independent pathways. We found GL-V9 can induce E2F-1 in the previous studies and speculate it may be a key point in regulation of E2F-1in the GL-V9-induced ER stress. We will examine the apoptotic effects of E2F-1 and influence factors regulating E2F-1 in the knocked-out CHOP, p53, p73 and E2F-1 cells treated with GL-V9; and study the interaction with E2F-1, P53 and MDM2, and examine degradation and sublocalization of P53 regulated by E2F-1. So we can explain and understand the apoptotic mechanism of wogonin in tumor therapy and provide a new strategy for wogonin in the drug research and development.