Evidence map›Paper›PMID 37233832›Full record

ArticleDiscover oncology2023

NEK2 promotes esophageal squamous cell carcinoma cell proliferation, migration and invasion through the Wnt/β-catenin signaling pathway.

Dong Guo, Weinan Yao, Xingyu Du, Jing Dong, Xueyuan Zhang, Wenbin Shen, Shuchai Zhu

Open access · goldAbstract read
In one paragraph

Article in Discover oncology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

7 citing papers in PubMed, 10 citations in OpenAlex.

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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

7 authors at 2 institutions in 1 country.

Dong GuoDepartment of Radiation Oncology, Fourth Hospital of Hebei Medical University, Shijiazhuang, 050000, China.
Weinan YaoDepartment of Radiation Oncology, Fourth Hospital of Hebei Medical University, Shijiazhuang, 050000, China.
Xingyu DuDepartment of Radiation Oncology, Fourth Hospital of Hebei Medical University, Shijiazhuang, 050000, China.
Jing DongDepartment of Radiation Oncology, Fourth Hospital of Hebei Medical University, Shijiazhuang, 050000, China.
Xueyuan ZhangDepartment of Radiation Oncology, Fourth Hospital of Hebei Medical University, Shijiazhuang, 050000, China.
Wenbin ShenDepartment of Radiation Oncology, Fourth Hospital of Hebei Medical University, Shijiazhuang, 050000, China.
Shuchai ZhuDepartment of Radiation Oncology, Fourth Hospital of Hebei Medical University, Shijiazhuang, 050000, China. shuchaizh1965@126.com.
Fourth Hospital of Hebei Medical University · CNHebei Medical University · CN

Funding

Medical Research Institute of Hebei Province 20221365National Natural Science Foundation of China No. 81872456Natural Science Foundation of China of Hebei Province No. H2020206583
6 · The paper itself

Abstract

objectivesThe NEK2 (never in mitosis gene A-related kinase 2), a serine/threonine kinase involved in chromosome instability and tumorigenesis. Hence, this study aimed to explore the molecular function of NEK2 in esophageal squamous cell carcinoma (ESCC).

methodsBy available transcriptome datasets (GSE53625 cohort, GSE38129 cohort, and GSE21293 cohort), we analyzed the differentially expressed genes in invading and non-invading ESCC. Subsequently, we evaluated the association between NEK2 expression level and clinical outcomes through Kaplan-Meier analysis method. The quantitative real-time polymerase chain reaction (qRT-PCR) and western blotting (WB) analyses were performed to determine the expression levels of NEK2 mRNA and protein, respectively. We knocked down the NEK2 expression in ESCC cells (ECA109 and TE1), and evaluated the NEK2 biology function associated with ESCC cell proliferation, migration, invasion, and colony formation abilities. Finally, the downstream pathway of NEK2 was analyzed through Gene Set Enrichment Analysis (GSEA) and validated the regulatory mechanism of NEK2 on the potential pathway through WB.

resultsWe found that NEK2 was highly expressed in ESCC cells compared with human esophageal epithelial cells (HEEC) (P < 0.0001), and high NEK2 expression was remarkably associated with poor survival (P = 0.019). Knockdown of NEK2 showed the significant inhibitory effect for tumorigenesis, and suppressed the ESCC cells proliferation, migration, invasion, and formation of colonies abilities. Additionally, GSEA revealed that Wnt/β-catenin pathway was a downstream pathway of NEK2. WB results further validated the regulatory mechanism of NEK2 for Wnt/β-catenin signaling.

conclusionsOur results indicated that NEK2 promotes ESCC cell proliferation, migration and invasion by activating the Wnt/β-catenin pathway. NEK2 could be a promising target for ESCC.

Indexed as

Esophageal squamous cell carcinomaInvasionNEK2ProliferationWnt/β-catenin

Identifiers

PMID37233832
PMCPMC10219921
OpenAlexW4378347851

What OpenQuestion holds

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Registered trials

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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.