Evidence map›Paper›PMID 19383899›Full record

ArticleCancer research2009

TGF-beta1 + EGF-initiated invasive potential in transformed human keratinocytes is coupled to a plasmin/MMP-10/MMP-1-dependent collagen remodeling axis: role for PAI-1.

Cynthia E Wilkins-Port, Qunhui Ye, Joseph E Mazurkiewicz, Paul J Higgins

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

40 citing papers in PubMed, 64 citations in OpenAlex.

  1. Article
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  11. The role of collagen in cancer: from bench to bedside.Journal of translational medicine · 2019
    Review
  12. Science advances · 2019
    Article
  13. Platelets Regulate Pulmonary Inflammation and Tissue Destruction in Tuberculosis.American journal of respiratory and critical care medicine · 2018
    Article
  14. Review
  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.

Cynthia E Wilkins-PortCenter for Cell Biology and Cancer Research, Albany Medical College, Albany, New York 12208, USA.
Qunhui Ye
Joseph E Mazurkiewicz
Paul J Higgins
Center for Cancer Research · USAlbany Medical Center Hospital · US

Funding

MATRIX MEDIATORS OF WOUND HEALINGR01GM057242 · NIGMS · WEILL MEDICAL COLLEGE OF CORNELL UNIV · PI HIGGINS, PAUL J. · 1998 to 2010
$3.2M
TISSUE REMODELING AND CARDIOVASCULAR DISEASET32HL007194 · NHLBI · ALBANY MEDICAL COLLEGE · PI MC KEOWN-LONGO, PAULA J · 1985 to 2006
$2.9M
NHLBI NIH HHS T32 HL007194NHLBI NIH HHS T32-HL07194NIGMS NIH HHS GM57242NIGMS NIH HHS R01 GM057242
6 · The paper itself

Abstract

The phenotypic switching called epithelial-to-mesenchymal transition is frequently associated with epithelial tumor cell progression from a comparatively benign to an aggressive, invasive malignancy. Coincident with the emergence of such cellular plasticity is an altered response to transforming growth factor-beta (TGF-beta) as well as epidermal growth factor (EGF) receptor amplification. TGF-beta in the tumor microenvironment promotes invasive traits largely through reprogramming gene expression, which paradoxically supports matrix-disruptive as well as stabilizing processes. ras-transformed HaCaT II-4 keratinocytes undergo phenotypic changes typical of epithelial-to-mesenchymal transition, acquire a collagenolytic phenotype, and effectively invade collagen type 1 gels as a consequence of TGF-beta1 + EGF stimulation in a three-dimensional physiologically relevant model system that monitors collagen remodeling. Enhanced collagen degradation was coupled to a significant increase in matrix metalloproteinase (MMP)-10 expression and involved a proteolytic axis composed of plasmin, MMP-10, and MMP-1. Neutralization of any one component in this cascade inhibited collagen gel lysis. Similarly, addition of plasminogen activator inhibitor type 1 (SERPINE1) blocked collagen degradation as well as the conversion of both proMMP-10 and proMMP-1 to their catalytically active forms. This study therefore identifies an important mechanism in TGF-beta1 + EGF-initiated collagen remodeling by transformed human keratinocytes and proposes a crucial upstream role for plasminogen activator inhibitor type 1-dependent regulation in this event.

Indexed as

Carcinoma, Squamous CellCell Line, TransformedCollagen Type IEpidermal Growth FactorFibrinolysinHumansKeratinocytesMatrix Metalloproteinase 1Matrix Metalloproteinase 10Plasminogen Activator Inhibitor 1Skin NeoplasmsTransforming Growth Factor beta1Collagen Type IEpidermal Growth FactorFibrinolysinMatrix Metalloproteinase 1Matrix Metalloproteinase 10Plasminogen Activator Inhibitor 1SERPINE1 protein, humanTransforming Growth Factor beta1

Identifiers

PMID19383899
PMCPMC2962982
OpenAlexW2030476631

What OpenQuestion holds

Textmetadata
LicenceTDM
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.