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目的 研究磷脂酰肌醇3 激酶(PI3K)和p42/p44丝裂源激活的蛋白激酶(MAPK)在 肝癌细胞血管内皮生长因子(VEGF)转录调控中的作用。方法 应用缺氧诱导剂氯化钴或重组人表 皮生长因子(EGF)刺激HepG2细胞中VEGF的转录,在此过程中应用PI3K特异性阻断剂 LY294002或p42/p44MAPK特异性阻断剂PD98059干预,采用半定量逆转录PCR检测VEGF mRNA表达的变化。结果 氯化钴或EGF可以诱导HepG2细胞中VEGF的表达。PI3K阻断剂 LY294002可以在一定范围内浓度依赖性地抑制VEGFmRNA的表达,而p42/p44MAPK阻断剂 PD98059对VEGFmRNA的表达无抑制作用。结论 肝癌细胞VEGF的转录调控受PI3K通路调 控,而不受p42/p44MAPK调控。
Objective To study the role of phosphatidylinositol 3-kinase (PI3K) and p42 / p44 mitogen-activated protein kinase (MAPK) in the transcriptional regulation of vascular endothelial growth factor (VEGF) in hepatocellular carcinoma cells. Methods The hypoxia-inducing agent cobalt chloride or recombinant human epidermal growth factor (EGF) was used to stimulate the transcription of VEGF in HepG2 cells. PI3K-specific inhibitor LY294002 or p42 / p44MAPK specific inhibitor PD98059 was used in this process. Semi-quantitative RT-PCR was used to detect the changes of VEGF mRNA expression. Results Cobalt chloride or EGF can induce the expression of VEGF in HepG2 cells. PI3K blocker LY294002 inhibited the expression of VEGF mRNA to a certain extent in a concentration-dependent manner, whereas p42 / p44 MAPK inhibitor PD98059 did not inhibit the expression of VEGF mRNA. Conclusion The transcriptional regulation of VEGF in hepatoma cells is regulated by PI3K pathway but not by p42 / p44MAPK.