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Erschienen in: Tumor Biology 12/2015

01.12.2015 | Review

The emerging role of Nemo-like kinase (NLK) in the regulation of cancers

verfasst von: Ying Huang, Yang Yang, Yong He, Jun Li

Erschienen in: Tumor Biology | Ausgabe 12/2015

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Abstract

Nemo-like kinase (NLK) is an evolutionarily conserved mitogen-activated protein (MAP) kinase-related kinase that is highly expressed in neural tissues and minimally detected in others. Accumulating evidence demonstrates that NLK exerts a pivotal role in cell proliferation, migration, invasion, and apoptosis via regulation of a variety of transcriptional molecules. The results of recent studies have shown that aberrant expression of NLK is significantly associated with the initiation and progression of various types of human cancers, as well as clinicopathologic features and survival rate. NLK is gradually considered as a potential tumor suppressor or an oncogene depending on the tumor system, and silencing or upregulating of NLK may provide an effective therapeutic approach against tumors. In this review, we will make a summary on the comprehensive roles of NLK in the regulation of various cancers.
Literatur
1.
Zurück zum Zitat Choi KW. Rotation of photoreceptor clusters in the developing Drosophila eye requires the nemo gene. Cell. 1994;78:125–36.CrossRefPubMed Choi KW. Rotation of photoreceptor clusters in the developing Drosophila eye requires the nemo gene. Cell. 1994;78:125–36.CrossRefPubMed
2.
3.
Zurück zum Zitat Katoh M. Comparative genomics on nemo-like kinase gene. Int J Oncol. 2005;26:1715–9.PubMed Katoh M. Comparative genomics on nemo-like kinase gene. Int J Oncol. 2005;26:1715–9.PubMed
4.
Zurück zum Zitat Kortenjann M. Abnormal bone marrow stroma in mice deficient for nemo-like kinase Nlk. Eur J Immunol. 2001;31:3580–7.CrossRefPubMed Kortenjann M. Abnormal bone marrow stroma in mice deficient for nemo-like kinase Nlk. Eur J Immunol. 2001;31:3580–7.CrossRefPubMed
5.
Zurück zum Zitat Ishitani T. Nemo-like kinase is involved in NGF-induced neurite outgrowth via phosphorylating MAP1B and paxillin. J Neurochem. 2009;111:1104–18.CrossRefPubMed Ishitani T. Nemo-like kinase is involved in NGF-induced neurite outgrowth via phosphorylating MAP1B and paxillin. J Neurochem. 2009;111:1104–18.CrossRefPubMed
6.
Zurück zum Zitat Xu D. Expression of Nemo-like kinase after spinal cord injury in rats. J Mol Neurosci. 2014;52:410–8.CrossRefPubMed Xu D. Expression of Nemo-like kinase after spinal cord injury in rats. J Mol Neurosci. 2014;52:410–8.CrossRefPubMed
7.
8.
Zurück zum Zitat Thorpe CJ. nemo-like kinase is an essential co-activator of Wnt signaling during early zebrafish development. Development. 2004;131:2899–909.CrossRefPubMed Thorpe CJ. nemo-like kinase is an essential co-activator of Wnt signaling during early zebrafish development. Development. 2004;131:2899–909.CrossRefPubMed
9.
Zurück zum Zitat Ishitani T. Nemo-like kinase, a multifaceted cell signaling regulator. Cell Signal. 2013;25:190–7.CrossRefPubMed Ishitani T. Nemo-like kinase, a multifaceted cell signaling regulator. Cell Signal. 2013;25:190–7.CrossRefPubMed
10.
Zurück zum Zitat Jung KH. Targeted disruption of Nemo-like kinase inhibits tumor cell growth by simultaneous suppression of cyclin D1 and CDK2 in human hepatocellular carcinoma. J Cell Biochem. 2010;110:687–96.CrossRefPubMed Jung KH. Targeted disruption of Nemo-like kinase inhibits tumor cell growth by simultaneous suppression of cyclin D1 and CDK2 in human hepatocellular carcinoma. J Cell Biochem. 2010;110:687–96.CrossRefPubMed
11.
Zurück zum Zitat Li M. Prognostic significance of nemo-like kinase (NLK) expression in patients with gallbladder cancer. Tumour Biol. 2013;34:3995–4000.CrossRefPubMed Li M. Prognostic significance of nemo-like kinase (NLK) expression in patients with gallbladder cancer. Tumour Biol. 2013;34:3995–4000.CrossRefPubMed
12.
13.
Zurück zum Zitat Zhang Y. Expression of NLK and its potential effect in ovarian cancer chemotherapy. Int J Gynecol Cancer. 2011;21:1380–7.CrossRefPubMed Zhang Y. Expression of NLK and its potential effect in ovarian cancer chemotherapy. Int J Gynecol Cancer. 2011;21:1380–7.CrossRefPubMed
14.
15.
Zurück zum Zitat Shaw-Hallgren G. Association of nuclear-localized Nemo-like kinase with heat-shock protein 27 inhibits apoptosis in human breast cancer cells. PLoS One. 2014;9:e96506.CrossRefPubMedPubMedCentral Shaw-Hallgren G. Association of nuclear-localized Nemo-like kinase with heat-shock protein 27 inhibits apoptosis in human breast cancer cells. PLoS One. 2014;9:e96506.CrossRefPubMedPubMedCentral
16.
Zurück zum Zitat Lv L. Nemo-like kinase (NLK) inhibits the progression of NSCLC via negatively modulating WNT signaling pathway. J Cell Biochem. 2014;115:81–92.CrossRefPubMed Lv L. Nemo-like kinase (NLK) inhibits the progression of NSCLC via negatively modulating WNT signaling pathway. J Cell Biochem. 2014;115:81–92.CrossRefPubMed
17.
Zurück zum Zitat Cui G. Clinical and biological significance of nemo-like kinase expression in glioma. J Clin Neurosci. 2011;18:271–5.CrossRefPubMed Cui G. Clinical and biological significance of nemo-like kinase expression in glioma. J Clin Neurosci. 2011;18:271–5.CrossRefPubMed
18.
Zurück zum Zitat Han Y. NLK, a novel target of miR-199a-3p, functions as a tumor suppressor in colorectal cancer. Biomed Pharmacother. 2014. Han Y. NLK, a novel target of miR-199a-3p, functions as a tumor suppressor in colorectal cancer. Biomed Pharmacother. 2014.
19.
Zurück zum Zitat Chen J. Nemo-like kinase expression predicts poor survival in colorectal cancer. Mol Med Rep. 2015;11:1181–7.PubMed Chen J. Nemo-like kinase expression predicts poor survival in colorectal cancer. Mol Med Rep. 2015;11:1181–7.PubMed
20.
Zurück zum Zitat Tan Z. NLK is a key regulator of proliferation and migration in gallbladder carcinoma cells. Mol Cell Biochem. 2012;369:27–33.CrossRefPubMed Tan Z. NLK is a key regulator of proliferation and migration in gallbladder carcinoma cells. Mol Cell Biochem. 2012;369:27–33.CrossRefPubMed
21.
Zurück zum Zitat Yasuda J. Nemo-like kinase induces apoptosis in DLD-1 human colon cancer cells. Biochem Biophys Res Commun. 2003;308:227–33.CrossRefPubMed Yasuda J. Nemo-like kinase induces apoptosis in DLD-1 human colon cancer cells. Biochem Biophys Res Commun. 2003;308:227–33.CrossRefPubMed
22.
Zurück zum Zitat Dong JR. Inhibition of nemo-like kinase increases taxol sensitivity in laryngeal cancer. Asian Pac J Cancer Prev. 2013;14:7137–41.CrossRefPubMed Dong JR. Inhibition of nemo-like kinase increases taxol sensitivity in laryngeal cancer. Asian Pac J Cancer Prev. 2013;14:7137–41.CrossRefPubMed
23.
Zurück zum Zitat Kohlhapp FJ. MicroRNAs as mediators and communicators between cancer cells and the tumor microenvironment. Oncogene. 2015. Kohlhapp FJ. MicroRNAs as mediators and communicators between cancer cells and the tumor microenvironment. Oncogene. 2015.
25.
Zurück zum Zitat Chen Z. The pivotal role of microRNA-155 in the control of cancer. J Cell Physiol. 2014;229:545–50.CrossRefPubMed Chen Z. The pivotal role of microRNA-155 in the control of cancer. J Cell Physiol. 2014;229:545–50.CrossRefPubMed
26.
Zurück zum Zitat Ji J. Identification of microRNA-181 by genome-wide screening as a critical player in EpCAM-positive hepatic cancer stem cells. Hepatology. 2009;50:472–80.CrossRefPubMedPubMedCentral Ji J. Identification of microRNA-181 by genome-wide screening as a critical player in EpCAM-positive hepatic cancer stem cells. Hepatology. 2009;50:472–80.CrossRefPubMedPubMedCentral
27.
Zurück zum Zitat Wang K. miR-92b controls glioma proliferation and invasion through regulating Wnt/beta-catenin signaling via Nemo-like kinase. Neuro Oncol. 2013;15:578–88.CrossRefPubMedPubMedCentral Wang K. miR-92b controls glioma proliferation and invasion through regulating Wnt/beta-catenin signaling via Nemo-like kinase. Neuro Oncol. 2013;15:578–88.CrossRefPubMedPubMedCentral
28.
Zurück zum Zitat Shen Q. MiR-101 functions as a tumor suppressor by directly targeting nemo-like kinase in liver cancer. Cancer Lett. 2014;344:204–11.CrossRefPubMed Shen Q. MiR-101 functions as a tumor suppressor by directly targeting nemo-like kinase in liver cancer. Cancer Lett. 2014;344:204–11.CrossRefPubMed
29.
Zurück zum Zitat Zou D. MiR-197 induces Taxol resistance in human ovarian cancer cells by regulating NLK. Tumour Biol. 2015. Zou D. MiR-197 induces Taxol resistance in human ovarian cancer cells by regulating NLK. Tumour Biol. 2015.
30.
Zurück zum Zitat Xu ZY. Knockdown of long non-coding RNA HOTAIR suppresses tumor invasion and reverses epithelial-mesenchymal transition in gastric cancer. Int J Biol Sci. 2013;9:587–97.CrossRefPubMedPubMedCentral Xu ZY. Knockdown of long non-coding RNA HOTAIR suppresses tumor invasion and reverses epithelial-mesenchymal transition in gastric cancer. Int J Biol Sci. 2013;9:587–97.CrossRefPubMedPubMedCentral
31.
Zurück zum Zitat Yang F. Long noncoding RNA CCAT1, which could be activated by c-Myc, promotes the progression of gastric carcinoma. J Cancer Res Clin Oncol. 2013;139:437–45.CrossRefPubMed Yang F. Long noncoding RNA CCAT1, which could be activated by c-Myc, promotes the progression of gastric carcinoma. J Cancer Res Clin Oncol. 2013;139:437–45.CrossRefPubMed
32.
Zurück zum Zitat Vernucci M. The H19 endodermal enhancer is required for Igf2 activation and tumor formation in experimental liver carcinogenesis. Oncogene. 2000;19:6376–85.CrossRefPubMed Vernucci M. The H19 endodermal enhancer is required for Igf2 activation and tumor formation in experimental liver carcinogenesis. Oncogene. 2000;19:6376–85.CrossRefPubMed
33.
Zurück zum Zitat Du Y. Elevation of highly up-regulated in liver cancer (HULC) by hepatitis B virus X protein promotes hepatoma cell proliferation via down-regulating p18. J Biol Chem. 2012;287:26302–11.CrossRefPubMedPubMedCentral Du Y. Elevation of highly up-regulated in liver cancer (HULC) by hepatitis B virus X protein promotes hepatoma cell proliferation via down-regulating p18. J Biol Chem. 2012;287:26302–11.CrossRefPubMedPubMedCentral
34.
35.
Zurück zum Zitat Martens-Uzunova ES. Long noncoding RNA in prostate, bladder, and kidney cancer. Eur Urol. 2014;65:1140–51.CrossRefPubMed Martens-Uzunova ES. Long noncoding RNA in prostate, bladder, and kidney cancer. Eur Urol. 2014;65:1140–51.CrossRefPubMed
36.
Zurück zum Zitat Zhang JX. HOTAIR, a cell cycle-associated long noncoding RNA and a strong predictor of survival, is preferentially expressed in classical and mesenchymal glioma. Neuro Oncol. 2013;15:1595–603.CrossRefPubMedPubMedCentral Zhang JX. HOTAIR, a cell cycle-associated long noncoding RNA and a strong predictor of survival, is preferentially expressed in classical and mesenchymal glioma. Neuro Oncol. 2013;15:1595–603.CrossRefPubMedPubMedCentral
37.
Zurück zum Zitat Zhou X. HOTAIR is a therapeutic target in glioblastoma. Oncotarget. 2015. Zhou X. HOTAIR is a therapeutic target in glioblastoma. Oncotarget. 2015.
38.
Zurück zum Zitat Takebe N. Targeting cancer stem cells by inhibiting Wnt, Notch, and Hedgehog pathways. Nat Rev Clin Oncol. 2011;8:97–106.CrossRefPubMed Takebe N. Targeting cancer stem cells by inhibiting Wnt, Notch, and Hedgehog pathways. Nat Rev Clin Oncol. 2011;8:97–106.CrossRefPubMed
39.
Zurück zum Zitat Gatcliffe TA. Wnt signaling in ovarian tumorigenesis. Int J Gynecol Cancer. 2008;18:954–62.CrossRefPubMed Gatcliffe TA. Wnt signaling in ovarian tumorigenesis. Int J Gynecol Cancer. 2008;18:954–62.CrossRefPubMed
40.
Zurück zum Zitat Ishitani T. Regulation of lymphoid enhancer factor 1/T-cell factor by mitogen-activated protein kinase-related Nemo-like kinase-dependent phosphorylation in Wnt/beta-catenin signaling. Mol Cell Biol. 2003;23:1379–89.CrossRefPubMedPubMedCentral Ishitani T. Regulation of lymphoid enhancer factor 1/T-cell factor by mitogen-activated protein kinase-related Nemo-like kinase-dependent phosphorylation in Wnt/beta-catenin signaling. Mol Cell Biol. 2003;23:1379–89.CrossRefPubMedPubMedCentral
41.
Zurück zum Zitat Yasuda J. Mammalian Nemo-like kinase enhances beta-catenin-TCF transcription activity in human osteosarcoma and neuroblastoma cells. Proc Jpn Acad Ser B Phys Biol Sci. 2007;83:16–25.CrossRefPubMedPubMedCentral Yasuda J. Mammalian Nemo-like kinase enhances beta-catenin-TCF transcription activity in human osteosarcoma and neuroblastoma cells. Proc Jpn Acad Ser B Phys Biol Sci. 2007;83:16–25.CrossRefPubMedPubMedCentral
42.
43.
Zurück zum Zitat Bender TP. Critical functions for c-Myb at three checkpoints during thymocyte development. Nat Immunol. 2004;5:721–9.CrossRefPubMed Bender TP. Critical functions for c-Myb at three checkpoints during thymocyte development. Nat Immunol. 2004;5:721–9.CrossRefPubMed
Metadaten
Titel
The emerging role of Nemo-like kinase (NLK) in the regulation of cancers
verfasst von
Ying Huang
Yang Yang
Yong He
Jun Li
Publikationsdatum
01.12.2015
Verlag
Springer Netherlands
Erschienen in
Tumor Biology / Ausgabe 12/2015
Print ISSN: 1010-4283
Elektronische ISSN: 1423-0380
DOI
https://doi.org/10.1007/s13277-015-4159-7

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