Evidence map›Paper›PMID 18567804›Full record

ArticleMolecular cancer research : MCR2008

Multiple signaling pathways are responsible for prostaglandin E2-induced murine keratinocyte proliferation.

Kausar M Ansari, Joyce E Rundhaug, Susan M Fischer

Open access · bronzeAbstract read
In one paragraph

Article in Molecular cancer research : MCR, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
4.0field-weighted citation impact, top 7% 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

37 citing papers in PubMed, 75 citations in OpenAlex.

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  9. Isookanin Inhibits PGEInternational journal of molecular sciences · 2021
    Article
  10. Hyaluronic acid promotes Lgr5American journal of physiology. Gastrointestinal and liver physiology · 2020
    Article
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  12. Review
  13. 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

3 authors at 1 institution in 1 country.

Kausar M AnsariScience Park-Research Division, The University of Texas M D Anderson Cancer Center, PO Box 389, Smithville, TX 78957, USA.
Joyce E Rundhaug
Susan M Fischer
The University of Texas MD Anderson Cancer Center · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
Pilot Project ProgramP30ES007784 · NIEHS · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI RICHIE, ELLEN R · 1996 to 2011
$16.4M
Mouse Models of Skin CancerU01CA105345 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI FISCHER, SUSAN M · 2004 to 2008
$4.2M
COX-2 in Skin CarcinogenesisR01CA100140 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI FISCHER, SUSAN M · 2003 to 2007
$1.7M
NCI NIH HHS CA100140NCI NIH HHS CA105345NCI NIH HHS CA16672NCI NIH HHS P30 CA016672NCI NIH HHS R01 CA100140NCI NIH HHS U01 CA105345NIEHS NIH HHS ES07784NIEHS NIH HHS P30 ES007784
6 · The paper itself

Abstract

Although prostaglandin E2 (PGE2) has been shown by pharmacologic and genetic studies to be important in skin cancer, the molecular mechanism(s) by which it contributes to tumor growth is not well understood. In this study, we investigated the mechanisms by which PGE2 stimulates murine keratinocyte proliferation using in vitro and in vivo models. In primary mouse keratinocyte cultures, PGE2 activated the epidermal growth factor receptor (EGFR) and its downstream signaling pathways as well as increased cyclic AMP (cAMP) production and activated the cAMP response element binding protein (CREB). EGFR activation was not significantly inhibited by pretreatment with a c-src inhibitor (PP2), nor by a protein kinase A inhibitor (H-89). However, PGE2-stimulated extracellularly regulated kinase 1/2 (ERK1/2) activation was completely blocked by EGFR, ERK1/2, and phosphatidylinositol 3-kinase (PI3K) pathway inhibitors. In addition, these inhibitors attenuated the PGE2-induced proliferation, nuclear factor-kappa B, activator protein-1 (AP-1), and CREB binding to the promoter regions of the cyclin D1 and vascular endothelial growth factor (VEGF) genes and expression of cyclin D1 and VEGF in primary mouse keratinocytes. Similarly, in vivo, we found that WT mice treated with PGE2 and untreated cyclooxygenase-2-overexpressing transgenic mice had higher levels of cell proliferation and expression of cyclin D1 and VEGF, as well as higher levels of activated EGFR, nuclear factor-kappa B, AP-1, and CREB, than vehicle-treated WT mice. Our findings provide evidence for a link between cyclooxygenase-2 overexpression and EGFR-, ERK-, PI3K-, cAMP-mediated cell proliferation, and the tumor-promoting activity of PGE2 in mouse skin.

Indexed as

Signal TransductionAnimalsCell ProliferationCells, CulturedCyclic AMPCyclic AMP-Dependent Protein KinasesCyclin D1DinoprostoneErbB ReceptorsKeratinocytesMiceMice, TransgenicMitogen-Activated Protein KinasesPhosphatidylinositol 3-KinasesProtein Kinase InhibitorsProto-Oncogene Proteins c-aktCyclic AMPCyclic AMP-Dependent Protein KinasesCyclin D1DinoprostoneErbB ReceptorsMitogen-Activated Protein KinasesPhosphatidylinositol 3-KinasesProtein Kinase InhibitorsProto-Oncogene Proteins c-aktProto-Oncogene Proteins pp60(c-src)Transcription FactorsVascular Endothelial Growth Factor A

Identifiers

PMID18567804
PMCPMC2759608
OpenAlexW2145125577

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.