缺氧通过诱导 Twist1 表达促进肝癌细胞上皮-间充质转化。
Hypoxia promotes epithelial-mesenchymal transition of hepatocellular carcinoma cells via inducing Twist1 expression.
机构信息
Department of Pathology, Liaocheng People's Hospital, Liaocheng, Shandong, P.R. China.
出版信息
Eur Rev Med Pharmacol Sci. 2017 Jul;21(13):3061-3068.
OBJECTIVE
To investigate whether hypoxia microenvironment induced hepatocellular carcinoma cells SMMC-7721 epithelial-mesenchymal transition (EMT) and to explore the underlying molecular mechanism.
MATERIALS AND METHODS
In this study, SMMC-7721 cells were cultured under normoxia and hypoxia conditions, respectively. RT-PCR and Western blot were used to monitor the expression level of EMT-related markers, E-cadherin, and vimentin, as well as hypoxia inducible factor-1α (HIF-1α) and Twist1. Then we performed the transwell invasion assays to detect the ability of cell invasion.
RESULTS
The results demonstrated that hypoxia micro-environment could induce hepatocellular carcinoma cells SMMC-7721 EMT and enhance the cell invasion ability. Furthermore, knockdown of Twist1 by using specific siRNA could reverse hypoxia-induced EMT process.
CONCLUSIONS
Hypoxia promotes hepatocellular carcinoma cells SMMC-7721 EMT by upregulating the expression of Twist1.
目的
探讨缺氧微环境是否诱导肝癌细胞 SMMC-7721 上皮-间充质转化（EMT），并探讨其潜在的分子机制。
材料与方法
本研究分别在常氧和缺氧条件下培养 SMMC-7721 细胞。采用 RT-PCR 和 Western blot 检测 EMT 相关标志物 E-钙黏蛋白和波形蛋白，以及缺氧诱导因子-1α（HIF-1α）和 Twist1 的表达水平。然后，我们进行了 Transwell 侵袭实验来检测细胞侵袭能力。
结果
结果表明，缺氧微环境可诱导肝癌细胞 SMMC-7721 EMT，并增强细胞侵袭能力。此外，使用特异性 siRNA 敲低 Twist1 可逆转缺氧诱导的 EMT 过程。
结论
缺氧通过上调 Twist1 的表达促进肝癌细胞 SMMC-7721 EMT。
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