Evidence map›Paper›PMID 25131192›Full record

ArticleScientific reports2014

NEK9-dependent proliferation of cancer cells lacking functional p53.

Daisuke Kurioka, Fumitaka Takeshita, Koji Tsuta, Hiromi Sakamoto, Shun-ichi Watanabe, Kenji Matsumoto, Masatoshi Watanabe, Hitoshi Nakagama, Takahiro Ochiya, Jun Yokota and 2 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.3field-weighted citation impact, top 19% 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

15 citing papers in PubMed, 18 citations in OpenAlex.

  1. Review
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  3. The emerging role of Never-in-Mitosis A - Related Kinases in the endothelium.The international journal of biochemistry & cell biology · 2024
    Review
  4. Article
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  6. In Mitosis You Are Not: The NIMA Family of Kinases inInternational journal of molecular sciences · 2022
    Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Somatic Mutations in NEK9 Cause Nevus Comedonicus.American journal of human genetics · 2016
    Article
  12. Article
  13. Article
  14. Article
  15. Article
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

12 authors at 5 institutions in 4 countries.

Daisuke Kurioka1] Division of Genome Biology, National Cancer Center Research Institute [2] Laboratory for Medical Engineering, Division of Materials and Chemical Engineering, Graduate School of Engineering, Yokohama National University, 79-1 Tokiwadai, Hodogaya-ku Yokohama 240-8501, Japan.
Fumitaka TakeshitaDivision of Molecular and Cellular Medicine, National Cancer Center Research Institute.
Koji TsutaDivision of Pathology and Clinical Laboratories, National Cancer Center Hospital, 5-1-1, Tsukiji, Chuo-ku Tokyo 104-0045.
Hiromi SakamotoDivision of Genetics, National Cancer Center Research Institute.
Shun-ichi WatanabeDivision of Thoracic Surgery, National Cancer Center Hospital, 5-1-1 Tsukiji, Chuo-ku Tokyo 104-0045.
Kenji MatsumotoDivision of Allergy &Immunology, National Research Institute for Child Health and Development, 2-10-1 Okura Setagaya-ku Tokyo, 157-8535.
Masatoshi WatanabeLaboratory for Medical Engineering, Division of Materials and Chemical Engineering, Graduate School of Engineering, Yokohama National University, 79-1 Tokiwadai, Hodogaya-ku Yokohama 240-8501, Japan.
Hitoshi NakagamaDivision of Cancer Development System, National Cancer Center Research Institute.
Takahiro OchiyaDivision of Molecular and Cellular Medicine, National Cancer Center Research Institute.
Jun Yokota1] Division of Genome Biology, National Cancer Center Research Institute [2] Institute of Predictive and Personalized Medicine of Cancer (IMPPC), Barcelona, Spain.
Takashi KohnoDivision of Genome Biology, National Cancer Center Research Institute.
Naoto TsuchiyaDivision of Genome Biology, National Cancer Center Research Institute.
National Cancer Research Institute · GBNational Cancer Center · USInstitute of Predictive and Personalized Medicine of Cancer · ESNational Center For Child Health and Development · JPYokohama National University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dysfunction of the p53 network is a major cause of cancer development, and selective elimination of p53-inactivated cancer cells therefore represents an ideal therapeutic strategy. In this study, we performed a microRNA target screen that identified NEK9 (NIMA-related kinase 9) as a crucial regulator of cell-cycle progression in p53-inactivated cancer cells. NEK9 depletion selectively inhibited proliferation in p53-deficient cancer cells both in vitro and in vivo. The resultant cell-cycle arrest occurred predominantly in G1 phase, and exhibited senescence-like features. Furthermore, NEK9 repression affected expression of a broad range of genes encoding cell-cycle regulators and factors involved in mRNA processing, suggesting a novel role for NEK9 in p53-deficient cells. Lung adenocarcinoma patients with positive staining for NEK9 and mutant p53 proteins exhibited significantly poorer prognoses, suggesting that expression of both proteins promotes tumor growth. Our findings demonstrate that a novel NEK9 network regulates the growth of cancer cells lacking functional p53.

Indexed as

AdenocarcinomaAdenocarcinoma of LungAnimalsCell Line, TumorCell ProliferationCellular SenescenceCyclin-Dependent Kinase Inhibitor p21FemaleG1 Phase Cell Cycle CheckpointsHumansLung NeoplasmsMiceMice, Inbred BALB CMice, NudeMicroRNAsMitogen-Activated Protein Kinase 14Cyclin-Dependent Kinase Inhibitor p21MicroRNAsMIRN22 microRNA, humanMitogen-Activated Protein Kinase 14NEK9 protein, humanNIMA-Related KinasesProtein Serine-Threonine KinasesRNA, Small InterferingTumor Suppressor Protein p53

Identifiers

PMID25131192
PMCPMC4135330
OpenAlexW1987298366

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.