Evidence map›Paper›PMID 30247800›Full record

ArticleJournal of cellular and molecular medicine2018

NEK4 kinase regulates EMT to promote lung cancer metastasis.

Nian-Hua Ding, Lu Zhang, Zhi Xiao, Zhuo-Xian Rong, Zhi Li, Jiang He, Lin Chen, Dan-Min Ou, Wei-Hua Liao, Lun-Quan Sun

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.1field-weighted citation impact, top 18% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

26 citing papers in PubMed, 35 citations in OpenAlex.

  1. Methylation-regulated tumor suppressor geneTranslational cancer research · 2025
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  5. The NIMA-related kinase family and cancer.Frontiers in oncology · 2025
    Review
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  7. The emerging role of Never-in-Mitosis A - Related Kinases in the endothelium.The international journal of biochemistry & cell biology · 2024
    Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 1 institution in 1 country.

Nian-Hua DingCenter for Molecular Medicine, Xiangya Hospital, Changsha, China.ORCID 0000-0002-6203-8464
Lu ZhangCenter for Molecular Medicine, Xiangya Hospital, Changsha, China.
Zhi XiaoDeparment of Breast Cancer Medicine, Xiangya Hospital, Central South University, Changsha, China.
Zhuo-Xian RongCenter for Molecular Medicine, Xiangya Hospital, Changsha, China.
Zhi LiCenter for Molecular Medicine, Xiangya Hospital, Changsha, China.
Jiang HeCenter for Molecular Medicine, Xiangya Hospital, Changsha, China.
Lin ChenCenter for Molecular Medicine, Xiangya Hospital, Changsha, China.
Dan-Min OuCenter for Molecular Medicine, Xiangya Hospital, Changsha, China.
Wei-Hua LiaoDepartment of Radiology, Xiangya Hospital, Changsha, China.
Lun-Quan SunCenter for Molecular Medicine, Xiangya Hospital, Changsha, China.ORCID 0000-0001-8887-1035
Central South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epithelial-to-mesenchymal transition (EMT) is a dynamic transitional state from the epithelial to mesenchymal phenotypes. Numerous studies have suggested that EMT and its intermediate states play important roles in tumor invasion and metastasis. To identify novel regulatory molecules of EMT, we screened a siRNA library targeting human 720 kinases in A549 lung adenocarcinoma cells harboring E-cadherin promoter-luciferase reporter vectors. NIMA-related kinase-4 (NEK4) was identified and characterized as a positive regulator of EMT in the screening. Suppression of NEK4 resulted in the inhibition of cell migration and invasion, accompanying with an increased expression of cell adhesion-related proteins such as E-cadherin and ZO1. Furthermore, NEK4 knockdown caused the decreased expression of the transcriptional factor Zeb1 and Smads proteins, which are known to play key roles in EMT regulation. Consistently, overexpression of NEK4 resulted in the decreased expression of E-cadherin and increased expression of Smad3. Using a mouse model with tail vein injection of NEK4 knockdown stable cell line, we found a lower rate of tumor formation and metastasis of the NEK4-knockdown cells in vivo. Thus, this study demonstrates NEK4 as a novel kinase involved in regulation of EMT and suggests that NEK4 may be further explored as a potential therapeutic target for lung cancer metastasis.

Indexed as

Epithelial-Mesenchymal TransitionA549 CellsAnimalsBiomarkers, TumorCadherinsCell MovementHumansLung NeoplasmsMCF-7 CellsMice, NudeNeoplasm MetastasisNIMA-Related KinasesSignal TransductionTranscription FactorsBiomarkers, TumorCadherinsNEK4 protein, humanNIMA-Related KinasesTranscription FactorsEMTinvasionlung cancermigrationNEK4

Identifiers

PMID30247800
PMCPMC6237562
OpenAlexW2893910941

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.