Evidence map›Paper›PMID 12856717›Full record

ArticleClinical & experimental metastasis2003

Modulation of glioma cell invasion and motility by adenoviral gene transfer of PAI-1.

G O Hjortland, K Bjørnland, S Pettersen, S S Garman-Vik, E Emilsen, J M Nesland, O Fodstad, O Engebraaten

Abstract read
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In one paragraph

Article in Clinical & experimental metastasis, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
1.8field-weighted citation impact, top 17% 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

15 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.

  1. Pooled it
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  4. Therapeutics targeting the fibrinolytic system.Experimental & molecular medicine · 2020
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  9. Breast cancer and metabolic syndrome linked through the plasminogen activator inhibitor-1 cycle.BioEssays : news and reviews in molecular, cellular and developmental biology · 2007
    Review
  10. Article
  11. Article
  12. Article
  13. Proteases and glioma angiogenesis.Brain pathology (Zurich, Switzerland) · 2005
    Review
  14. Article
  15. 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

8 authors at 3 institutions in 1 country.

G O HjortlandDepartment of Tumor Biology, Institute for Cancer Research, The Norwegian Radium Hospital, University of Oslo, Montebello, Oslo, Norway. g.o.hjortland@labmed.uio.no
K Bjørnland
S Pettersen
S S Garman-Vik
E Emilsen
J M Nesland
O Fodstad
O Engebraaten
University of Oslo · NONorwegian Cancer Society · NOOslo University Hospital · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A number of studies have emphasized the role of PAI-1 as an important regulator of tumor cell invasion and metastasis. The hallmark of primary tumors of the central nervous system and glioblastomas in particular is the diffuse invasion into the normal brain tissue. Since PAI-1 is expressed in such tumors, we studied the effect of adenoviral-mediated transfer of the PAI-1 gene in regulating the in vitro invasiveness of D54Mg glioma cells into Matrigel, and into fetal rat brain aggregates. Treatment of D54Mg cells with 50 MOI (multiplicity of infection) of the replication defective vector AdCMVPAI-1 increased PAI-1 expression 23-fold compared to control vectors, and the invasion through Matrigel was reduced by 67%. The motility of the cells was reduced by 58% compared to controls (indicating that inhibition of motility was the principal effect of PAI-1 in these cells). The ability of D54Mg tumor spheroids to invade fetal rat brain aggregates was not reduced by the PAI-1 gene transfer. The results show that overexpression of PAI-1 can inhibit glioma cell motility and invasion through extracellular matrix (ECM) components, like laminin and collagen, but does not inhibit tumor cell invasion in a three-dimensional invasion assay, simulating normal brain tissue having a different ECM and interstitial composition. The different results obtained in the two invasion assays reflect the complex biological effects of the uPA/PAI-1 system, and questions a simplistic view of PAI- I as an inhibitor of brain tumor invasion.

Indexed as

Gene Transfer TechniquesAdenoviridaeAnimalsBlotting, NorthernBrain NeoplasmsCell AdhesionCell MovementCollagenDrug CombinationsEnzyme-Linked Immunosorbent AssayFetusGenetic VectorsGliomaHumansImmunoenzyme TechniquesLamininCollagenDrug CombinationsLamininmatrigelPlasminogen Activator Inhibitor 1ProteoglycansSerine Proteinase Inhibitors

Identifiers

PMID12856717
OpenAlexW2074475484

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.