【作者】 刘爱华；

【导师】 伍钢；

【作者基本信息】 华中科技大学 ， 肿瘤学， 2010， 硕士

【摘要】 目的:肿瘤组织中的缺氧微环境启动肿瘤血管形成,但其具体机制尚不明了。本实验以A549人肺癌细胞,HepG2人肝癌细胞为研究对象,探讨不同缺氧时间后,Plexin B1这一与血管生成密切相关的基因表达情况;方法:设置对照组和实验组,分别采用细胞免疫荧光法和Real-time PCR法观察在不同缺氧时间后肿瘤细胞内Plexin B1的表达变化;结果:细胞免疫荧光实验显示Plexin B1荧光信号定位于细胞膜上,缺氧条件下,Plexin B1基因表达明显强于常氧组,缺氧18小时达高峰;Real-time PCR实验结果与细胞免疫荧光实验结果一致;结论:缺氧可以诱导Plexin B1表达,表达量随缺氧时间的延长而升高,18小时达高峰,提示Plexin B1上调可能参与缺氧诱导的血管生成。更多还原

【Abstract】 Objective: The hypoxic tumor microenvironment induced angiogenesis, but the specific mechanism was unclear. In this experiment, A549 human lung cancer cells, HepG2 human liver cancer cells were studied, to investigate the expression of Plexin B1, which was relevant with tumor angiogenesis, under different hypoxia condition.Methods: Cells cultured in hypoxia conditions and normoxia condition, and then analyzed the difference expression of Plexin B1 with different hypoxia time within the tumor cells by immunofluorescence and Real-time PCR assay.Results: Immunofluorescence showed that the signal of Plexin B1 located on cellular membrane and Plexin B1 expression up-regulated in hypoxic condition and reached peak until hypoxic keeping on 18 hours. The result of Real-time PCR is same with immunofluorescence.Conclusion: Hypoxic can induce Plexin B1 expression, and the expression increases as the persistence of hypoxic, which cued that Plexin B1 up-regulation may particpate the progression of hypoxia-mediated angiogenesis.更多还原