[α-烯醇化酶（ENO1）通过抑制ERK1/2磷酸化来抑制A549细胞系中的上皮-间质转化]
[α-Enolase (ENO1) inhibits epithelial-mesenchymal transition in the A549 cell line by suppressing ERK1/2 phosphorylation].
作者信息
Zhou Xin, Zhang Ying, Han Naijun, Guo Suping, Xiao Ting, Cheng Shujun, Gao Yanning, Zhang Kaitai
机构信息
State Key Laboratory of Molecular Oncology, Beijing Key Laboratory of Carcinogenesis and Cancer Prevention, Cancer Institute, Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100021, China.
出版信息
Zhongguo Fei Ai Za Zhi. 2013 May;16(5):221-6. doi: 10.3779/j.issn.1009-3419.2013.05.01.
BACKGROUND AND OBJECTIVE
It has been proven that epithelial-mesenchymal transition (EMT) is a critical process which is precisely regulated by multiple signaling pathways during the progression and metastasis of non-small cell lung cancer (NSCLC). Canonical MAPK signaling is essential to transforming growth factor β (TGFβ)-induced EMT. Using the NSCLC cell line A549 as a model, the aim of this study is to explore the molecular mechanism of ENO1 affecting EMT.
METHODS
We established an A549 strain stably overexpressing ENO1. Cell mobility was measured by the wound-healing assay. EMT-related molecular alterations were detected by Western blot analysis. The effect of ENO1 on EMT was also detected by TGFβ-1-inducing assay. EGF-stimulating assay was performed to illustrate ERK1/2 phosphorylation changes resulting from ENO1 overexpression.
RESULTS
Overexpressed ENO1 inhibited the mobility of A549 (P<0.05), as well as the expression of the mesenchymal markers N-cadherin and vimentin, but upregulated the epithelial marker E-cadherin. TGFβ-inducing assay also showed that the negative effect of ENO1 on EMT. ERK1/2 phosphorylation was also obviously suppressed by ENO1 in the EGF-stimulating assay.
CONCLUSIONS
In NSCLC cells, ENO1 overexpression can inhibit EMT in vitro by suppressing ERK1/2 phosphorylation.
背景与目的
业已证实，上皮-间质转化（EMT）是一个关键过程，在非小细胞肺癌（NSCLC）的进展和转移过程中受到多种信号通路的精确调控。经典的丝裂原活化蛋白激酶（MAPK）信号对于转化生长因子β（TGFβ）诱导的EMT至关重要。本研究以NSCLC细胞系A549为模型，旨在探讨ENO1影响EMT的分子机制。
方法
我们建立了稳定过表达ENO1的A549细胞株。通过伤口愈合试验检测细胞迁移能力。采用蛋白质免疫印迹分析检测EMT相关分子变化。通过TGFβ-1诱导试验检测ENO1对EMT的影响。进行表皮生长因子（EGF）刺激试验以阐明ENO1过表达导致的细胞外信号调节激酶1/2（ERK1/2）磷酸化变化。
结果
过表达的ENO1抑制了A549细胞的迁移能力（P<0.05），以及间充质标志物N-钙黏蛋白和波形蛋白的表达，但上调了上皮标志物E-钙黏蛋白的表达。TGFβ诱导试验也表明ENO1对EMT具有负面影响。在EGF刺激试验中，ENO1也明显抑制了ERK1/2磷酸化。
结论
在NSCLC细胞中，ENO1过表达可通过抑制ERK1/2磷酸化在体外抑制EMT。
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