| 摘要: |
| 目的:观察bevacizumab对肝癌细胞株HepG2增殖的影响，并探讨其可能的作用机制。方法:应用免疫细胞化学法和RT-PCR分别从蛋白和基因水平检测肝癌细胞株HepG2中血管内皮生长因子(VEGF)及其受体Flt-1、KDR的表达；ELISA检测HepG2培养上清液中VEGF蛋白的浓度；人重组VEGF(rhVEGF)和bevacizumab分别处理HepG2细胞后，MTT法检测细胞增殖活性，应用RT-PCR和Western印迹分别从基因和蛋白水平检测VEGF表达量的变化。结果:HepG2细胞中VEGF、Flt-1和KDR蛋白均呈阳性表达。rhVEGF可促进HepG2细胞的增殖，在0~100 ng/ml区间其促进增殖的作用呈剂量依赖性；而bevacizumab可抑制HepG2细胞的增殖，浓度为0.1、1、10、20 μg/ml时细胞增殖抑制率分别为(8.76%±1.15)%、(26.83±1.20)%、(31.87±1.30)%、(28.20±1.28)%。rhVEGF可促进HepG2细胞中VEGF的表达，而bevacizumab能抑制VEGF的表达。结论:Bevacizumab可能通过阻断VEGF的促增殖作用而抑制HepG2细胞增殖。 |
| 关键词: 肝细胞癌 HepG2细胞株 bevacizumab 血管内皮生长因子类 |
| DOI：10.3724/SP.J.1008.2008.01060 |
| 投稿时间：2008-03-25修订日期：2008-06-17 |
| 基金项目: |
|
| Antiangiogenesis agent bevacizumab blocks the promoting effect of vascular endothelial growth factor on proliferation of human hepatoma cell line HepG2 |
| WAN Cheng1,2，CUI Fei1，CHEN Bin1，LUO Rong-cheng1* |
| (1.Tumor Center，Nanfang Hospital，Southern Medical University，Guangzhou 510515,China*2.Affiliated Drum Tower Hospital,Medical School of Nanjing University,Nanjing 210008) |
| Abstract: |
| Objective:To observe the effect of bevacizumab on the proliferation of human heptoma cell line HepG2. Methods: The expression of vascular endothelial growth factor(VEGF) and its receptors (VEGFRs) in HepG2 cells were examined by immunocytochemical staining and RT-PCR；ELISA was used to determine the level of VEGF in culture supernatants of HepG2 cells. The proliferation of HepG2 cells was analyzed by MTT assay after treatment with rhVEGF and bevacizumab separately; the expression of VEGF was examined by RT-PCR and Western blotting. Results: VEGF and VEGFRs (Flt-1 and KDR) were expressed in human HepG2 cells. rhVEGF increased the proliferation of HepG2 cells in a dose-dependent manner within a concentration range of 0-100 ng/ml; bevacizumab inhibited the proliferation of HepG2 cells; the inhibition rates were (8.76%±1.15)%,(26.83±1.20)%,(31.87±1.30)% and (28.20±1.28)%, when the concentrations of bevacizumab were 0.1,1,10,and 20 μg/ml,respectively. Expression of VEGF in the HepG2 cells was increased by rhVEGF and inhibited by bevacizumab. Conclusion: Bevacizumab might inhibit the proliferation of HepG2 cells through blocking the effect of VEGF. |
| Key words: hepatocellular carcinoma HepG2 cell line bevacizumab vascular endothelial growth factors |
