Lentivirus-mediated knockdown of NLK inhibits small-cell lung cancer growth and metastasis

Lv, Mutian; Li, Yaming; Tian, Xin; Dai, Shun‐Dong; Sun, Jing; Jin, Guojiang; Jiang, Shenyi

doi:10.2147/dddt.s87435

Cited by 8 publications

(3 citation statements)

References 24 publications

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“…Moreover, misregulation of Nmo-like kinases in humans, namely an increase in Nmo levels, has been correlated with various cancers 80 , 81 , which together might suggest that Nmo generally regulates tissue fluidity and that dysregulation of tissue fluidity can have a negative impact in disease 54 , including cancer 73 . The unjamming transition has been proposed to resemble invasion of interstitial spaces by tumor cells, particularly those that are not dependent upon epithelial-mesenchymal transition 56 .…”

Section: Discussionmentioning

confidence: 99%

Tissue fluidity mediated by adherens junction dynamics promotes planar cell polarity-driven ommatidial rotation

et al. 2021

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The phenomenon of tissue fluidity—cells’ ability to rearrange relative to each other in confluent tissues—has been linked to several morphogenetic processes and diseases, yet few molecular regulators of tissue fluidity are known. Ommatidial rotation (OR), directed by planar cell polarity signaling, occurs during Drosophila eye morphogenesis and shares many features with polarized cellular migration in vertebrates. We utilize in vivo live imaging analysis tools to quantify dynamic cellular morphologies during OR, revealing that OR is driven autonomously by ommatidial cell clusters rotating in successive pulses within a permissive substrate. Through analysis of a rotation-specific nemo mutant, we demonstrate that precise regulation of junctional E-cadherin levels is critical for modulating the mechanical properties of the tissue to allow rotation to progress. Our study defines Nemo as a molecular tool to induce a transition from solid-like tissues to more viscoelastic tissues broadening our molecular understanding of tissue fluidity.

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Section: Discussionmentioning

confidence: 99%

Tissue fluidity mediated by adherens junction dynamics promotes planar cell polarity-driven ommatidial rotation

et al. 2021

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“…Investigations into gallbladder cancer demonstrated that NLK was upregulated in cancer tissues, which was associated with the poor prognosis of patients (28). Notably, Lv et al reported that increased NLK expression in SCLC could promote invasion and metastasis (29). Conversely, the present study observed reduced NLK expression in NSCLC; this may reflect the differential expression of NLK in organs, tissues and the internal environment of cells (30).…”

Section: Discussionmentioning

confidence: 99%

Knockdown of Nemo‑like kinase promotes metastasis in non‑small‑cell lung cancer

Shi

Tang

et al. 2019

Oncol Rep

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The evolutionarily conserved serine/threonine kinase Nemo-like kinase (NLK) serves an important role in cell proliferation, migration, invasion and apoptosis by regulating transcription factors among various cancers. In the present study, the function of NLK in human non-small cell lung cancer (NSCLC) was investigated. Immunohistochemical analysis and western blotting demonstrated that NLK expression was significantly reduced in NSCLC tissues compared with corresponding peritumoral tissues. Statistical analysis revealed that decreased NLK expression was associated with the presence of primary tumors, tumor node metastasis (TNM) staging, differentiation, lymph node metastasis, and E-cadherin and vimentin expression. Univariate analysis indicated that NLK expression, differentiation, lymph node metastasis, TNM stage, and E-cadherin and vimentin expression affected the prognosis of NSCLC. Cox regression analyses revealed NLK expression and TNM as independent factors that affected prognosis. Kaplan-Meier survival analysis revealed that patients with NSCLC and low NLK expression had relatively shorter durations of overall survival. In vitro , NLK overexpression inhibited A549 ncell migration and invasion as determined by wound healing and Transwell migration assays, respectively. Additionally, immunofluorescence staining indicated that downregulation of NLK expression could induce epithelial-mesenchymal transition in NSCLC. NLK knockdown significantly decreased the expression of the epithelial marker E-cadherin, and markedly increased that of β-catenin and the mesenchymal marker vimentin. Furthermore, NLK was reported to directly interact with β-catenin as determined by a co-immunoprecipitation assay. Collectively, the results of the present study indicated that decreased NLK expression could promote tumor metastasis in NSCLC.

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“…Yet, Lv et al 26 reported that low NLK expression was an independent prognostic factor for NSCLC patients’ low survival rate by multivariate analysis. However, Lv et al 27 revealed that lentivirus-mediated knockdown of NLK inhibits small-cell lung cancer growth and metastasis. These suggest that the same gene NLK may function differently in the location of histology and cytology.…”

Section: Discussionmentioning

confidence: 99%

Expression of Nemo-like kinase in cervical squamous cell carcinoma: a clinicopathological study

Yang

et al. 2018

OTT

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ObjectiveNemo-like kinase (NLK) has been reported to play different roles in tumors. However, the role of NLK in cervical squamous cell carcinoma (CSCC) remains unknown. In this study, we explored the clinical significance including survival of NLK protein expression in CSCCs.Patients and methodsImmunohistochemical method was performed using tissues from 130 patients with CSCC. The associations between NLK expression and the clinicopathological factors and prognosis of CSCCs were evaluated. Statistical analyses were performed using the chi-square test, the multivariate Cox proportional hazard model, and the Kaplan–Meier method.ResultsImmunohistochemical staining analysis showed that NLK was localized predominately in the nucleus of the tumor cells, and increased NLK expression was detected in 71 (54.6%) of 130 patients. NLK overexpression significantly correlated with higher histological grade (P=0.001), vascular/lymphatic invasion (P=0.010), lymph node metastasis (P=0.012), and recurrence (P=0.022). Patients with elevated NLK expression had poorer overall survival (OS) and disease-free survival (DFS) (P=0.006 and P=0.004, respectively) compared with patients with decreased NLK expression. Multivariate Cox analysis demonstrated that NLK overexpression was an independent factor for OS and DFS (P=0.034 and P=0.025, respectively).ConclusionNLK may be a valuable biomarker for predicting the prognosis of CSCC patients and may serve as a potential target for cancer therapy.

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Lentivirus-mediated knockdown of NLK inhibits small-cell lung cancer growth and metastasis

Cited by 8 publications

References 24 publications

Tissue fluidity mediated by adherens junction dynamics promotes planar cell polarity-driven ommatidial rotation

Tissue fluidity mediated by adherens junction dynamics promotes planar cell polarity-driven ommatidial rotation

Knockdown of Nemo‑like kinase promotes metastasis in non‑small‑cell lung cancer

Expression of Nemo-like kinase in cervical squamous cell carcinoma: a clinicopathological study

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