Evidence map›Paper›PMID 19604388›Full record

ArticleMolecular cancer2009

Breast cancer cells stimulate osteoprotegerin (OPG) production by endothelial cells through direct cell contact.

Penny E Reid, Nicola J Brown, Ingunn Holen

Open access · goldAbstract read
In one paragraph

Article in Molecular cancer, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
0.9field-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

17 citing papers in PubMed, 43 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Upregulation of osteoprotegerin inhibitsExperimental and therapeutic medicine · 2022
    Article
  5. Review
  6. Ascites from Ovarian Cancer Induces Novel Fucosylated Proteins.Cancer microenvironment : official journal of the International Cancer Microenvironment Society · 2019
    Article
  7. RANK-RANKL Signaling in Cancer of the Uterine Cervix: A Review.International journal of molecular sciences · 2019
    Review
  8. Estrogen deficiency impairs integrin αScientific reports · 2019
    Article
  9. Osteoprotegerin Induces CD34Frontiers in medicine · 2018
    Article
  10. Review
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. 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

3 authors at 1 institution in 1 country.

Penny E ReidAcademic Units of Clinical Oncology and Surgical Oncology, School of Medicine and Biomedical Sciences, University of Sheffield, Sheffield, UK. p.reid@sheffield.ac.uk
Nicola J Brown
Ingunn Holen
University of Sheffield · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAngiogenesis, the sprouting of capillaries from existing blood vessels, is central to tumour growth and progression, however the molecular regulation of this process remains to be fully elucidated. The secreted glycoprotein osteoprotegerin (OPG) is one potential pro-angiogenic factor, and clinical studies have demonstrated endothelial cells within a number of tumour types to express high levels of OPG compared to those in normal tissue. Additionally, OPG can increase endothelial cell survival, proliferation and migration, as well as induce endothelial cell tube formation in vitro. This study aims to elucidate the processes involved in the pro-angiogenic effects of OPG in vitro, and also how OPG levels may be regulated within the tumour microenvironment.

resultsIt has previously been demonstrated that OPG can induce tube formation on growth factor reduced matrigel. In this study, we demonstrate that OPG enhances the pro-angiogenic effects of VEGF and that OPG does not stimulate endothelial cell tube formation through activation of the VEGFR2 receptor. We also show that cell contact between HuDMECs and the T47D breast cancer cell line increases endothelial cell OPG mRNA and protein secretion levels in in vitro co-cultures. These increases in endothelial cell OPG secretion were dependent on alphanubeta3 ligation and NFkappaB activation. In contrast, the pro-angiogenic factors VEGF, bFGF and TGFbeta had no effect on HuDMEC OPG levels.

conclusionThese findings suggest that the VEGF signalling pathway is not involved in mediating the pro-angiogenic effects of OPG on endothelial cells in vitro. Additionally, we show that breast cancer cells cause increased levels of OPG expression by endothelial cells, and that direct contact between endothelial cells and tumour cells is required in order to increase endothelial OPG expression and secretion. Stimulation of OPG secretion was shown to involve alphanubeta3 ligation and NFkappaB activation.

Indexed as

Analysis of VarianceBreast NeoplasmsCell CommunicationCell Line, TumorEndothelial CellsFemaleHumansIntegrin alphaVbeta3Neovascularization, PathologicNF-kappa BOsteoprotegerinTumor Cells, CulturedTumor Necrosis Factor-alphaVascular Endothelial Growth Factor AVascular Endothelial Growth Factor Receptor-2Integrin alphaVbeta3NF-kappa BOsteoprotegerinTumor Necrosis Factor-alphaVascular Endothelial Growth Factor AVascular Endothelial Growth Factor Receptor-2VEGFA protein, human

Identifiers

PMID19604388
PMCPMC2719583
OpenAlexW2128953767

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.