Evidence map›Paper›PMID 19436306›Full record

ArticleBritish journal of cancer2009

Bacterial endotoxin enhances colorectal cancer cell adhesion and invasion through TLR-4 and NF-kappaB-dependent activation of the urokinase plasminogen activator system.

S D Killeen, J H Wang, E J Andrews, H P Redmond

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed, 1 pooled it
3.8field-weighted citation impact, top 6% 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

50 citing papers in PubMed, 1 synthesis or guideline pooled it, 104 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Betulinic acid and obesity-related disorders.Frontiers in pharmacology · 2025
    Review
  5. Review
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  9. Microbiota in colorectal cancer related to liver metastasis.Chinese journal of cancer research = Chung-kuo yen cheng yen chiu · 2024
    Article
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  11. Article
  12. Review
  13. Review
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  15. 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

4 authors at 2 institutions in 1 country.

S D KilleenDepartment of Academic Surgery, Cork University Hospital and University College Cork, Cork, Ireland. sdfkilleen@eircom.net
J H Wang
E J Andrews
H P Redmond
Cork University Hospital · IEUniversity College Cork · IE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Perioperative exposure to lipopolysaccharide (LPS) is associated with accelerated metastatic colorectal tumour growth. LPS directly affects cells through Toll-like receptor 4 (TLR-4) and the transcription factor NF-kappaB. The urokinase plasminogen activator (u-PA) system is intimately implicated in tumour cell extracellular matrix (ECM) interactions fundamental to tumour progression. Thus we sought to determine if LPS directly induces accelerated tumour cell ECM adhesion and invasion through activation of the u-PA system and to elucidate the cellular pathways involved. Human colorectal tumour cell lines were stimulated with LPS. u-PA concentration, u-PA activity, active u-PA, surface urokinase plasminogen activator receptor (u-PAR) and TLR-4 expression were assessed by ELISA, colorimetric assay, western blot analysis and flow cytometry respectively. In vitro tumour cell vitronectin adhesion and ECM invasion were analysed by vitronectin adhesion assay and ECM invasion chambers. u-PA and u-PAR function was inhibited with anti u-PA antibodies or the selective u-PA inhibitors amiloride or WXC-340, TLR-4 by TLR-4-blocking antibodies and NF-kappaB by the selective NF-kappaB inhibitor SN-50. LPS upregulates u-PA and u-PAR in a dose-dependent manner, enhancing in vitro tumour cell vitronectin adhesion and ECM invasion by >40% (P<0.01). These effects were ameliorated by u-PA and u-PAR inhibition. LPS activates NF-kappaB through TLR-4. TLR-4 and NF-kappaB inhibition ameliorated LPS-enhanced u-PA and u-PAR expression, tumour cell vitronectin adhesion and ECM invasion. LPS promotes tumour cell ECM adhesion and invasion through activation of the u-PA system in a TLR-4- and NF-kappaB-dependent manner.

Indexed as

AmilorideAntibodiesBacterial ToxinsCaco-2 CellsCarcinomaCell AdhesionCell MovementColorectal NeoplasmsHumansLipopolysaccharidesNeoplasm InvasivenessNF-kappa BReceptors, Urokinase Plasminogen ActivatorToll-Like Receptor 4Tumor Cells, CulturedUrokinase-Type Plasminogen ActivatorAmilorideAntibodiesBacterial ToxinsLipopolysaccharidesNF-kappa BReceptors, Urokinase Plasminogen ActivatorTLR4 protein, humanToll-Like Receptor 4Urokinase-Type Plasminogen Activator

Identifiers

PMID19436306
PMCPMC2696751
OpenAlexW2020061008

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.