Evidence map›Paper›PMID 18058029›Full record

ArticleClinical & experimental metastasis2008

Nm23-H1 homologs suppress tumor cell motility and anchorage independent growth.

William G McDermott, Mathieu Boissan, Marie-Lise Lacombe, Patricia S Steeg, Christine E Horak

Abstract read
PubMed Publisher
In one paragraph

Article in Clinical & experimental metastasis, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
1.1field-weighted citation impact, top 25% 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

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.

  1. Pooled it
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  6. The mitochondrial nucleoside diphosphate kinase (NDPK-D/NME4), a moonlighting protein for cell homeostasis.Laboratory investigation; a journal of technical methods and pathology · 2018
    Review
  7. Characterization of a group I Nme protein of Capsaspora owczarzaki-a close unicellular relative of animals.Laboratory investigation; a journal of technical methods and pathology · 2018
    Article
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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

5 authors at 4 institutions in 3 countries.

William G McDermottWomen's Cancers Section, Laboratory of Molecular Pharmacology, Center for Cancer Research, National Cancer Institute, NCI/NIH, 37 Convent Dr., Bethesda, MD 20892, USA.
Mathieu Boissan
Marie-Lise Lacombe
Patricia S Steeg
Christine E Horak
Center for Cancer Research · USInserm · FRNational Cancer Institute · MYSorbonne Université · FR

Funding

Molecular Biology of the Metastatic PhenotypeZIASC000892 · NCI · DIVISION OF CLINICAL SCIENCES - NCI · PI STEEG, PATRICIA SCHRIVER · 2009 to 2023
$8.4M
MOLECULAR BIOLOGY OF THE METASTATIC PHENOTYPEZ01SC000892 · SC · DIVISION OF CLINICAL SCIENCES - NCI · PI STEEG, PATRICIA SCHRIVER · 1996 to 2008
$1.3M
Intramural NIH HHS
6 · The paper itself

Abstract

Nm23-H1 suppresses metastasis, as well as in vitro cell motility, invasion and anchorage independent growth, in a variety of cancer models. Eight human homologs of Nm23 have been identified that share 26-88% identity with the prototype Nm23-H1. Here, we examine the potential of its homologs, -H2, DR-, -H4 and -H5, to inhibit in vitro correlates of metastasis in two highly metastatic human cell lines, MDA-MB-435 and MDA-MB-231. The metastatic cells were transfected with mammalian expression constructs containing the genes encoding for Nm23-H1, -H2, DR-, -H4 and -H5 and the resultant transfectants were analyzed by Boyden chamber motility and soft agar colonization assays. Nm23-H1 suppressed motility by 3.3- and 1.5-fold in MDA-MB-435 and MDA-MB-231 cells, respectively and inhibited anchorage independent growth in soft agar by 2.9- and 1.9-fold, respectively. None of the -H1 homologs were capable of suppressing motility in MDA-MB-435 cells, but in MDA-MB-231 cells, -H2 inhibited motility by 3-fold upon overexpression. When anchorage independent growth was assessed, -H2, -H4 and -H5 suppressed growth from 1.2- to 2.0-fold in both cell lines. Given their ability to suppress anchorage independent growth, Nm23-H1 homologs -H2, -H4 and -H5 may have some capacity to suppress metastasis. Motility suppression appears to be cell context dependent, but sequence disparities between -H1/H2 and the other family members may reveal regions critical for this inhibitory phenotype. Similarly, sequence differences between DR-Nm23 and its homologs may be important for anchorage independent growth suppression.

Indexed as

Amino Acid SequenceCell Line, TumorCell MovementFemaleHumansMolecular Sequence DataNeoplasm MetastasisNM23 Nucleoside Diphosphate KinasesSequence Homology, Amino AcidTransfectionNM23 Nucleoside Diphosphate KinasesNME1 protein, human

Identifiers

PMID18058029
OpenAlexW2037457503

What OpenQuestion holds

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Read underepoch 390

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.