Evidence map›Paper›PMID 21505453›Full record

ArticleBritish journal of cancer2011

A role for nucleotides in support of breast cancer angiogenesis: heterologous receptor signalling.

N Yokdang, J D Tellez, H Tian, J Norvell, S H Barsky, M Valencik, I L O Buxton

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
0.7field-weighted citation impact, top 31% 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

16 citing papers in PubMed, 35 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. The mJournal of experimental & clinical cancer research : CR · 2019
    Article
  8. The 'known-knowns', and 'known-unknowns' of extracellular Nm23-H1/NDPK proteins.Laboratory investigation; a journal of technical methods and pathology · 2018
    Review
  9. Review
  10. Extracellular NME proteins: a player or a bystander?Laboratory investigation; a journal of technical methods and pathology · 2018
    Review
  11. Article
  12. Article
  13. Purinergic signalling and cancer.Purinergic signalling · 2013
    Review
  14. Review
  15. Article
  16. 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

7 authors at 1 institution in 1 country.

N YokdangDepartment of Pharmacology, Centre for Molecular Medicine, University of Nevada School of Medicine, Mail Stop 573, Reno, NV 89557, USA.
J D Tellez
H Tian
J Norvell
S H Barsky
M Valencik
I L O Buxton
University of Nevada, Reno · US

Funding

REGULATION OF MYOMETRIAL RELAXATION: AGONIST-SPECIFIC cGMP ACTIONR01HD053028 · NICHD · UNIVERSITY OF NEVADA RENO · PI BUXTON, IAIN L · 2007 to 2011
$1.4M
NCRR NIH HHS P20 RR1581NICHD NIH HHS HD053028NICHD NIH HHS R01 HD053028
6 · The paper itself

Abstract

backgroundHuman breast carcinoma cells secrete an adenosine 5'-diphosphate transphosphorylase (sNDPK) known to induce endothelial cell tubulogenesis in a P2Y receptor-dependent manner. We examined sNDPK secretion and its effects on human endothelial cells.

methodsNucleoside diphosphate kinase (NDPK) secretion was measured by western blot and enzyme-linked immunosorbent assay, while transphosphorylase activity was measured using the luciferin-luciferase ATP assay. Activation of MAPK was determined by western blot analysis, immunofluorescence and endothelial cell proliferation and migration.

resultsA panel of breast cancer cell lines with origin as ductal carcinoma, adenocarcinoma or medullary carcinoma, secrete sNDPK-A/B. Addition of purified NDPK-B to endothelial cultures activated VEGFR-2 and Erk(1/2), both of which were blocked by inhibitors of NDPK and P2Y receptors. Activation of VEGFR-2 and ErK(1/2) by 2-methylthio-ATP (2MeS-ATP) was blocked by pretreatment with the P2Y(1)-specific antagonist MRS2179, the proto-oncogene non-receptor tyrosine kinase (Src) inhibitor PP2 or the VEGFR-2 antagonist SU1498. Nucleoside diphosphate kinase-B stimulates cell growth and migration in a concentration-dependent manner comparable to the effect of vascular endothelial growth factor. Treatment of endothelial cells with either NDPK-B or 2MeS-ATP induced migration, blocked by P2Y(1), Src or VEGFR-2 antagonists.

conclusionsNDPK supports angiogenesis. Understanding the mechanism of action of sNDPK and P2Y(1) nucleotide signalling in metastasis and angiogenesis represent new therapeutic targets for anti-angiogenic therapies to benefit patients.

Indexed as

Breast NeoplasmsCell Growth ProcessesCell Line, TumorEndothelial CellsFemaleHumansNeovascularization, PathologicNucleoside-Diphosphate KinaseNucleotidesPhosphorylationProto-Oncogene MasSignal TransductionTumor Cells, CulturedVascular Endothelial Growth Factor Receptor-2MAS1 protein, humanNucleoside-Diphosphate KinaseNucleotidesProto-Oncogene MasVascular Endothelial Growth Factor Receptor-2

Identifiers

PMID21505453
PMCPMC3101911
OpenAlexW2088118861

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.