Evidence map›Paper›PMID 21460252›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2011

AMP kinase-related kinase NUAK2 affects tumor growth, migration, and clinical outcome of human melanoma.

Takeshi Namiki, Atsushi Tanemura, Julio C Valencia, Sergio G Coelho, Thierry Passeron, Masakazu Kawaguchi, Wilfred D Vieira, Masashi Ishikawa, Wataru Nishijima, Toshiyuki Izumo and 11 more

Abstract readMulticenter Study
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
1.5field-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

40 citing papers in PubMed, 60 citations in OpenAlex.

  1. Review
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  4. Diagnostics (Basel, Switzerland) · 2025
    Article
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  6. A fetal oncogene NUAK2 is an emerging therapeutic target in glioblastoma.bioRxiv : the preprint server for biology · 2025
    Article
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  12. Review
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  19. AMPKα-like proteins as LKB1 downstream targets in cell physiology and cancer.Journal of molecular medicine (Berlin, Germany) · 2021
    Review
  20. 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

21 authors at 7 institutions in 2 countries.

Takeshi NamikiLaboratory of Cell Biology, National Cancer Institute, Bethesda, MD 20814, USA.
Atsushi Tanemura
Julio C Valencia
Sergio G Coelho
Thierry Passeron
Masakazu Kawaguchi
Wilfred D Vieira
Masashi Ishikawa
Wataru Nishijima
Toshiyuki Izumo
Yasuhiko Kaneko
Ichiro Katayama
Yuji Yamaguchi
Lanlan Yin
Eric C Polley
Hongfang Liu
Yutaka Kawakami
Yoshinobu Eishi
Eishi Takahashi
Hiroo Yokozeki
Vincent J Hearing
State Key Laboratory of Cell BiologyNational Institutes of Health · USSaitama Cancer Center · JPTokyo Medical and Dental University · JPOsaka University · JPKeio University · JPNational Cancer Institute · US

Funding

Characterization of Pigmentary Disorders and Melanoma TargetingZIABC010785 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI HEARING, VINCENT J · 2009 to 2014
$3.0M
Onto-BioThesaurus: ontological representation of gene/protein names for biomedicaR01LM009959 · NLM · MAYO CLINIC ROCHESTER · PI LIU, HONGFANG · 2009 to 2010
$1.2M
Intramural NIH HHSNLM NIH HHS R01 LM009959
6 · The paper itself

Abstract

The identification of genes that participate in melanomagenesis should suggest strategies for developing therapeutic modalities. We used a public array comparative genomic hybridization (CGH) database and real-time quantitative PCR (qPCR) analyses to identify the AMP kinase (AMPK)-related kinase NUAK2 as a candidate gene for melanomagenesis, and we analyzed its functions in melanoma cells. Our analyses had identified a locus at 1q32 where genomic gain is strongly associated with tumor thickness, and we used real-time qPCR analyses and regression analyses to identify NUAK2 as a candidate gene at that locus. Associations of relapse-free survival and overall survival of 92 primary melanoma patients with NUAK2 expression measured using immunohistochemistry were investigated using Kaplan-Meier curves, log rank tests, and Cox regression models. Knockdown of NUAK2 induces senescence and reduces S-phase, decreases migration, and down-regulates expression of mammalian target of rapamycin (mTOR). In vivo analysis demonstrated that knockdown of NUAK2 suppresses melanoma tumor growth in mice. Survival analysis showed that the risk of relapse is greater in acral melanoma patients with high levels of NUAK2 expression than in acral melanoma patients with low levels of NUAK2 expression (hazard ratio = 3.88; 95% confidence interval = 1.44-10.50; P = 0.0075). These data demonstrate that NUAK2 expression is significantly associated with the oncogenic features of melanoma cells and with the survival of acral melanoma patients. NUAK2 may provide a drug target to suppress melanoma progression. This study further supports the importance of NUAK2 in cancer development and tumor progression, while AMPK has antioncogenic properties.

Indexed as

Cell MovementGene Expression Regulation, EnzymologicGene Expression Regulation, NeoplasticAnimalsCellular SenescenceDisease-Free SurvivalFemaleGene Knockdown TechniquesGenetic LociGenome-Wide Association StudyHumansMaleMelanomaMiceMice, NudeNeoplasm ProteinsMTOR protein, humanNeoplasm ProteinsNUAK2 protein, humanProtein Serine-Threonine KinasesTOR Serine-Threonine Kinases

Identifiers

PMID21460252
PMCPMC3081019
OpenAlexW2045048651

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.