Evidence map›Paper›PMID 22080566›Full record

ArticleCancer research2012

Metastasis suppressor NM23-H1 promotes repair of UV-induced DNA damage and suppresses UV-induced melanomagenesis.

Stuart G Jarrett, Marian Novak, Sandrine Dabernat, Jean-Yves Daniel, Isabel Mellon, Qingbei Zhang, Nathan Harris, Michael J Ciesielski, Robert A Fenstermaker, Diane Kovacic and 2 more

Open access · greenAbstract read
In one paragraph

Article in Cancer research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

39 citing papers in PubMed, 56 citations in OpenAlex.

  1. Article
  2. Article
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  4. Histidine Phosphorylation: Protein Kinases and Phosphatases.International journal of molecular sciences · 2024
    Review
  5. Long-chain fatty acyl coenzyme A inhibits NME1/2 and regulates cancer metastasis.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  6. Review
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  18. The NDPK/NME superfamily: state of the art.Laboratory investigation; a journal of technical methods and pathology · 2018
    Article
  19. Nuclear functions of NME proteins.Laboratory investigation; a journal of technical methods and pathology · 2018
    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

12 authors at 4 institutions in 2 countries.

Stuart G JarrettDepartment of Molecular and Biomedical Pharmacology, and Graduate Center for Toxicology, University of Kentucky College of Medicine and Markey Cancer Center, Lexington, Kentucky 40536, USA.
Marian Novak
Sandrine Dabernat
Jean-Yves Daniel
Isabel Mellon
Qingbei Zhang
Nathan Harris
Michael J Ciesielski
Robert A Fenstermaker
Diane Kovacic
Andrzej Slominski
David M Kaetzel
Inserm · FRThe Graduate Center, CUNY · USUniversity of Tennessee Health Science Center · USUniversity of Kentucky · US

Funding

NM23 PROTEINS AND MECHANISMS OF PDGF A CHAIN SILENCINGR01CA083237 · NCI · UNIVERSITY OF KENTUCKY · PI KAETZEL, DAVID M · 1999 to 2010
$1.9M
NCI NIH HHS CA83237NCI NIH HHS R01 CA083237
6 · The paper itself

Abstract

Reduced expression of the metastasis suppressor NM23-H1 is associated with aggressive forms of multiple cancers. Here, we establish that NM23-H1 (termed H1 isoform in human, M1 in mouse) and two of its attendant enzymatic activities, the 3'-5' exonuclease and nucleoside diphosphate kinase, are novel participants in the cellular response to UV radiation (UVR)-induced DNA damage. NM23-H1 deficiency compromised the kinetics of repair for total DNA polymerase-blocking lesions and nucleotide excision repair of (6-4) photoproducts in vitro. Kinase activity of NM23-H1 was critical for rapid repair of both polychromatic UVB/UVA-induced (290-400 nm) and UVC-induced (254 nm) DNA damage, whereas its 3'-5' exonuclease activity was dominant in the suppression of UVR-induced mutagenesis. Consistent with its role in DNA repair, NM23-H1 rapidly translocated to sites of UVR-induced (6-4) photoproduct DNA damage in the nucleus. In addition, transgenic mice hemizygous-null for nm23-m1 and nm23-m2 exhibited UVR-induced melanoma and follicular infundibular cyst formation, and tumor-associated melanocytes displayed invasion into adjacent dermis, consistent with loss of invasion-suppressing activity of NM23 in vivo. Taken together, our data show a critical role for NM23 isoforms in limiting mutagenesis and suppressing UVR-induced melanomagenesis.

Indexed as

DNA DamageUltraviolet RaysAnimalsCell Line, TumorHypoxanthine PhosphoribosyltransferaseMelanoma, ExperimentalMiceMice, Inbred C57BLMutationNeoplasms, Radiation-InducedNM23 Nucleoside Diphosphate KinasesHypoxanthine PhosphoribosyltransferaseNM23 Nucleoside Diphosphate Kinases

Identifiers

PMID22080566
PMCPMC3251703
OpenAlexW2147338798

What OpenQuestion holds

Textmetadata
LicenceTDM
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.