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首页> 外文期刊>Anticancer Research: International Journal of Cancer Research and Treatment >Human EAG1 potassium channels in the epithelial-to-mesenchymal transition in lung cancer cells.
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Human EAG1 potassium channels in the epithelial-to-mesenchymal transition in lung cancer cells.

机译：人EAG1钾通道在肺癌细胞的上皮到间质转化中。

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摘要

BACKGROUND: Human ether a go-go-1 (EAG1) potassium channels are potential tools for cancer diagnosis, prognosis and therapy. Epithelial-to-mesenchymal transition (EMT) is a likely mechanism by which tumor cells become malignant. We wondered whether EAG1 is regulated in human lung tumor cells undergoing EMT. MATERIALS AND METHODS: EMT was induced in A549 lung tumor cells with transforming growth factor beta (TGFbeta1). EAG1 gene expression was assesed by real-time RT-PCR and protein expression by flow cytometry. RESULTS: TGFbeta1 produced the expected changes in morphology, migration and gene expression associated to EMT. EAG1 gene and protein expression were up-regulated during EMT. Astemizole did not prevent EMT. CONCLUSION: Our results suggest that EAG1 channels participate in the acquisition of a malignant phenotype in lung tumor cells. Their potential role in EMT might not be uniquely related to their conducting function, in accordance with the reported tumor growth supported by non-conducting EAG1 channels.
机译：背景：人类以gogo-go-1（EAG1）钾通道是癌症诊断，预后和治疗的潜在工具。上皮到间质转化（EMT）是肿瘤细胞恶变的可能机制。我们想知道EAG1在经历EMT的人肺肿瘤细胞中是否受到调节。材料与方法：转化生长因子β（TGFbeta1）在A549肺肿瘤细胞中诱导EMT。通过实时RT-PCR评估EAG1基因表达，并通过流式细胞术评估蛋白质表达。结果：TGFbeta1产生与EMT相关的形态，迁移和基因表达的预期变化。在EMT期间EAG1基因和蛋白质表达上调。阿司咪唑没有预防EMT。结论：我们的结果表明，EAG1通道参与了肺肿瘤细胞恶性表型的获得。根据非传导性EAG1通道支持的报道的肿瘤生长，它们在EMT中的潜在作用可能与其传导功能并非唯一相关。

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