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当代肿瘤药物靶点

Editor-in-Chief

ISSN (Print): 1568-0096
ISSN (Online): 1873-5576

Research Article

Nemo样激酶的过度表达促进肺癌细胞的增殖和侵袭,并表明预后不良

卷 19, 期 8, 2019

页: [674 - 680] 页: 7

弟呕挨: 10.2174/1568009618666181119150521

价格: $65

摘要

背景:Nemo样激酶(NLK)是一种进化上保守的MAP激酶相关激酶,参与几种人类癌症的发病机制。 目的:本研究旨在探讨NLK在肺癌中的表达及作用及其机制。 方法:我们通过蛋白质印迹分析检测了肺癌组织中NLK的表达。 我们分别通过基因转染或RNA干扰增强或敲低了肺癌细胞中的NLK表达,并检测了Wnt信号通路和上皮 - 间质转化(EMT)中关键蛋白的表达改变。 我们还通过细胞增殖,集落形成和基质胶侵袭测定检查了NLK在肺癌细胞增殖和侵袭中的作用。 结果:发现肺癌组织样品中的NLK表达显着高于相应的健康肺组织样品。 NLK的过度表达与肺癌患者的预后不良相关。 NLK的过表达上调β-连环蛋白,TCF4和Wnt靶基因,例如细胞周期蛋白D1,c-Myc和MMP7。 N-cadherin和TWIST是EMT中的关键蛋白,被上调,而E-钙粘蛋白表达减少。 另外,在NLK过表达细胞中,增殖,集落形成和入侵被证实是增强的。 在NLK敲低肺癌细胞后,我们获得了相反的结果。 结论:NLK在肺癌中过度表达,预示着预后不良。 NLK的过表达激活Wnt信号传导途径和EMT并促进肺癌细胞的增殖和侵袭。

关键词: Nemo样激酶,肺癌,wnt信号通路,上皮 - 间质转化,增殖,侵袭。

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