Evidence map›Paper›PMID 32761510›Full record

ArticleMolecular and cellular biochemistry2020

High expression of NEK2 promotes lung cancer progression and drug resistance and is regulated by mutant EGFR.

Chuanhui Chen, Shanshan Peng, Penghui Li, Lin Ma, Xin Gan

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular and cellular biochemistry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.2field-weighted citation impact, top 10% 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

13 citing papers in PubMed, 21 citations in OpenAlex.

  1. Role of NEK2 in tumorigenesis and tumor progression.Trends in molecular medicine · 2025
    Review
  2. The emerging role of Never-in-Mitosis A - Related Kinases in the endothelium.The international journal of biochemistry & cell biology · 2024
    Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. In Mitosis You Are Not: The NIMA Family of Kinases inInternational journal of molecular sciences · 2022
    Review
  8. Article
  9. Article
  10. NcRNA-Mediated High Expression ofFrontiers in oncology · 2022
    Article
  11. Article
  12. The Hypoxia-Long Noncoding RNA Interaction in Solid Cancers.International journal of molecular sciences · 2021
    Review
  13. Review
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

5 authors at 1 institution in 1 country.

Chuanhui ChenDepartment of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Nanchang University, No. 17 Yongwaizheng Street, Nanchang, 330006, Jiangxi, People's Republic of China.
Shanshan PengDepartment of Healthy, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, People's Republic of China.
Penghui LiDepartment of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Nanchang University, No. 17 Yongwaizheng Street, Nanchang, 330006, Jiangxi, People's Republic of China.
Lin MaDepartment of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Nanchang University, No. 17 Yongwaizheng Street, Nanchang, 330006, Jiangxi, People's Republic of China.
Xin GanDepartment of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Nanchang University, No. 17 Yongwaizheng Street, Nanchang, 330006, Jiangxi, People's Republic of China. xganncu@outlook.com.ORCID http://orcid.org/0000-0001-8917-5795
Nanchang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Activating mutations within the tyrosine kinase (TK) domain of epidermal growth factor receptor (EGFR) gene are observed in 10 ~ 30% of the patients diagnosed with non-small cell lung cancer (NSCLC), and are causally related to NSCLC initiation and progression. Treatments with tyrosine kinase inhibitors (TKIs) targeting EGFR significantly improve the outcome of NSCLC patients with EGFR mutation, but are often associated with drug resistance, which is the main cause of treatment failure and cancer relapse. In the present study, by screening the transcriptome of NSCLC patients, we found that EGFR activation is highly correlated with the up-regulation of mitotic regulator, never in mitosis gene A-related kinase 2 (NEK2). NEK2 overexpression is associated with the poor survival of EGFR-mutant patients but not the wild-type patients. Further functional validation revealed that EGFR mutation induces NEK2 expression by activating ERK signaling pathway. Elevated NEK2 level promotes the rapid cell cycle progression and favors the rapid proliferation of EGFR-mutant NSCLC cells. Of note, NEK2 overexpression also impairs the efficacy of TKI treatment via inhibiting apoptosis, while depleting NEK2 suppresses cell growth and restored the sensitivity of TKI in NSCLC cells. Taken together, our study revealed that NEK2 is an oncogene regulated by EGFR mutation and is involved in disease progression and treatment response in NSCLC with EGFR mutation. These findings will pave the road for optimizing personalized treatment strategies to overcome drug resistance and improve the prognosis of lung cancer patients with EGFR mutation.

Indexed as

MutationCarcinoma, Non-Small-Cell LungCell Line, TumorCell ProliferationDatabases, GeneticDisease ProgressionDrug Resistance, NeoplasmErbB ReceptorsHumansLung NeoplasmsNeoplasm Recurrence, LocalNIMA-Related KinasesPrognosisSignal TransductionSurvival RateEGFR protein, humanErbB ReceptorsNEK2 protein, humanNIMA-Related KinasesCell proliferationEGFR mutationGefitinib resistanceNEK2Non-small cell lung cancer

Identifiers

PMID32761510
OpenAlexW3047405714

What OpenQuestion holds

Textmetadata
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.