论文部分内容阅读
目的构建缺氧诱导模型和观察缺氧对人结肠癌SW480细胞系缺氧诱导因子-1α(HIF-1α)和Survivin基因表达的影响。方法利用氯化钴(CoCl_2)构建缺氧诱导模型；利用逆转录-聚合酶链反应(RT-PCR)分别测定CoCl_2缺氧诱导与SW480细胞HIF-1α和Survivin基因mRNA表达的时效关系(0、2、4、8、24 h)和量效关系(0、50、100、150、200μmol/L)。结果HIF-1α和Sur- vivin基因mRNA表达与氯化钴浓度呈明显的剂量依赖关系；HIF-1α基因表达随诱导时间的延长而逐渐增强,4 h亚组出现一个表达高峰,Survivin基因在缺氧诱导4 h呈现表达最高峰；HIF-1α与Survivin基因mRNA的表达在缺氧诱导量效关系(r=0．521,P＜0．05)和时效关系(r=0．693,P＜0．05)中均呈显著正相关。结论缺氧可以诱导HIF-1α和Survivin基因的表达增加；HIF-1α与Survivin基因的表达均呈显著相关,提示Survivin基因可能与HIF-1α存在某种调控关系并在缺氧抗凋亡机制中发挥作用。
Objective To construct hypoxia-induced model and observe the effects of hypoxia on the expression of hypoxia-inducible factor-1α (HIF-1α) and Survivin gene in human colon cancer SW480 cell line. Methods The hypoxia-inducible model was constructed using cobalt chloride (CoCl 2 ); the time-effect relationship between hypoxia-induced CoCl 2 and HIF-1α and Survivin mRNA expression in SW480 cells was determined by reverse transcription-polymerase chain reaction (RT-PCR). 2, 4, 8, 24 h) and dose-effect relationships (0, 50, 100, 150, 200 μmol/L). Results The mRNA expression of HIF-1α and sur-vinvin showed a dose-dependent relationship with the concentration of cobalt chloride. The expression of HIF-1α gene gradually increased with the prolongation of induction time, and there was a peak expression in the 4 h subgroup. The Survivin gene was absent. Oxygen induced peak expression at 4 h; HIF-1α and Survivin mRNA expression in response to hypoxia (r=0.521, P<0.05) and time-dependent relationship (r=0.693, P< There was a significant positive correlation in 0.05). Conclusion Hypoxia can induce the increase of HIF-1α and Survivin gene expression; HIF-1α and Survivin gene expression are significantly correlated, suggesting that Survivin gene may have a certain regulatory relationship with HIF-1α and in the mechanism of hypoxia and anti-apoptosis Play a role.