Evidence map›Paper›PMID 11571649›Full record

ArticleOncogene2001

VEGF(165) requires extracellular matrix components to induce mitogenic effects and migratory response in breast cancer cells.

T Miralem, R Steinberg, D Price, H Avraham

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

19 citing papers in PubMed, 60 citations in OpenAlex.

  1. Review
  2. Article
  3. Engineering a High-Throughput 3-D In Vitro Glioblastoma Model.IEEE journal of translational engineering in health and medicine · 2015
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. A catalytic role of heparin within the extracellular matrix.The Journal of biological chemistry · 2008
    Article
  12. Article
  13. Article
  14. The role of VEGF receptors in angiogenesis; complex partnerships.Cellular and molecular life sciences : CMLS · 2006
    Review
  15. Article
  16. Article
  17. Fibronectin Mechanobiology Regulates Tumorigenesis.Cellular and molecular bioengineering
    Review
  18. Article
  19. Review
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

4 authors at 1 institution in 1 country.

T MiralemDivision of Experimental Medicine, Beth Israel-Deaconess Medical Center, Harvard Institutes of Medicine, 4 Blackfan Circle, Boston, Massachusetts, MA 02115, USA.
R Steinberg
D Price
H Avraham
Beth Israel Deaconess Medical Center · US

Funding

CHK, NOVEL SIGNALING MOLECULE, IN BREAST CANCERR01CA076226 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI AVRAHAM, HAVA KARSENTY · 1999 to 2002
$810k
RELATED ADHESION KINASE IN MEGAKARYOCYTESR01HL055445 · NHLBI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI AVRAHAM, SHALOM · 1996 to 2000
$385k
NCI NIH HHS CA76226NHLBI NIH HHS HL55445NIAMS NIH HHS AR21 CA 87290-01
6 · The paper itself

Abstract

The expression of VEGF and the relapse-free survival rate of breast cancer patients are inversely related. While VEGF induces the proliferation and migration of vascular endothelial cells, its function in breast cancer cells is not well studied. We reported previously that fibronectin increased VEGF-dependent migration in breast cancer cells. Since VEGF has an extracellular matrix (ECM)-binding domain and possesses binding affinity for heparin, we sought to determine the effects of VEGF in breast cancer cells and the role of heparin and/or fibronectin in VEGF-induced signaling. Cells grown on plastic were compared to those grown on fibronectin or to those grown on plastic in the presence of heparin, and analysed for intracellular signaling, proliferation and migration in response to VEGF(165). Both heparin and fibronectin enhanced the binding of VEGF to T47D cells. After treatment with VEGF, [(3)H]thymidine incorporation, c-fos induction, and the number of migrating cells were significantly higher ( approximately twofold) in cells grown on fibronectin or in cells grown on plastic in the presence of heparin when compared to those grown on plastic only. Likewise, tyrosine phosphorylation of VEGF receptors, MAPK activity and PI3-kinase activity were all several-fold higher in cells seeded on fibronectin or in the presence of heparin as compared to cells exposed to VEGF alone. VEGF-dependent c-fos induction was found to be regulated through a MAPK-dependent, but PI3-kinase-independent pathway. In contrast, the migration of T47D cells in response to VEGF, in the presence of ECM, was regulated through PI3-kinase. Therefore, VEGF requires ECM components to induce a mitogenic response and cell migration in T47D breast cancer cells.

Indexed as

Neoplasm InvasivenessBreast NeoplasmsCell DivisionCell MovementDNAEndothelial Growth FactorsExtracellular MatrixFemaleFibronectinsHeparinHumansLymphokinesMitogen-Activated Protein Kinase 1Phosphatidylinositol 3-KinasesProto-Oncogene Proteins c-fosRNA, NeoplasmDNAEndothelial Growth FactorsFibronectinsHeparinLymphokinesMitogen-Activated Protein Kinase 1Phosphatidylinositol 3-KinasesProto-Oncogene Proteins c-fosRNA, NeoplasmVascular Endothelial Growth Factor AVascular Endothelial Growth FactorsVEGFA protein, human

Identifiers

PMID11571649
OpenAlexW2318901649

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.