Department of Pathology, The First Hospital and College of Basic Medical Sciences, China Medical University, Shenyang 110001, China.
100K80B, Clinical Medicine of Seven-year Programme, China Medical University, Shenyang 110001, China.
Curr Cancer Drug Targets. 2019;19(8):674-680. doi: 10.2174/1568009618666181119150521.
Nemo-like kinase (NLK) is an evolutionarily conserved MAP kinaserelated kinase involved in the pathogenesis of several human cancers.
The aim of this study was to investigate the expression and role of NLK in lung cancers, and its underlying mechanisms.
We examined the expression of NLK in lung cancer tissues through western blot analysis. We enhanced or knocked down NLK expression by gene transfection or RNA interference, respectively, in lung cancer cells, and examined expression alterations of key proteins in the Wnt signaling pathway and in epithelial-mesenchymal transition (EMT). We also examined the roles of NLK in the proliferation and invasiveness of lung cancer cells by cell proliferation, colony formation, and Matrigel invasion assays.
NLK expression was found to be significantly higher in lung cancer tissue samples than in corresponding healthy lung tissue samples. Overexpression of NLK correlated with poor prognosis of patients with lung cancer. Overexpression of NLK upregulated β-catenin, TCF4, and Wnt target genes such as cyclin D1, c-Myc, and MMP7. N-cadherin and TWIST, the key proteins in EMT, were upregulated, while E-cadherin expression was reduced. Additionally, proliferation, colony formation, and invasion turned out to be enhanced in NLK-overexpressing cells. After NLK knockdown in lung cancer cells, we obtained the opposite results.
NLK is overexpressed in lung cancers and indicates poor prognosis. Overexpression of NLK activates the Wnt signaling pathway and EMT and promotes the proliferation and invasiveness of lung cancer cells.
Nemo 样激酶（NLK）是一种进化上保守的丝氨酸/苏氨酸激酶，与多种人类癌症的发病机制有关。
本研究旨在探讨 NLK 在肺癌中的表达和作用及其潜在机制。
我们通过 Western blot 分析检测了肺癌组织中 NLK 的表达。通过基因转染或 RNA 干扰分别增强或敲低肺癌细胞中的 NLK 表达，检测 Wnt 信号通路和上皮-间质转化（EMT）中关键蛋白的表达变化。我们还通过细胞增殖、集落形成和 Matrigel 侵袭实验研究了 NLK 在肺癌细胞增殖和侵袭中的作用。
NLK 的表达在肺癌组织样本中明显高于相应的健康肺组织样本。NLK 的过表达与肺癌患者的预后不良相关。NLK 的过表达上调了β-catenin、TCF4 和 Wnt 靶基因，如 cyclin D1、c-Myc 和 MMP7。EMT 的关键蛋白 N-钙黏蛋白和 TWIST 上调，而 E-钙黏蛋白表达下调。此外，NLK 过表达细胞的增殖、集落形成和侵袭能力增强。在肺癌细胞中敲低 NLK 后，我们得到了相反的结果。
NLK 在肺癌中过度表达，预示着预后不良。NLK 的过表达激活了 Wnt 信号通路和 EMT，促进了肺癌细胞的增殖和侵袭。
