Evidence map›Paper›PMID 18362203›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2008

Transcriptional and post-transcriptional mechanisms for lysophosphatidic acid-induced cyclooxygenase-2 expression in ovarian cancer cells.

Regina A Oyesanya, Zendra P Lee, Jinhua Wu, Jing Chen, Yuanda Song, Abir Mukherjee, Paul Dent, Tomasz Kordula, Huiping Zhou, Xianjun Fang

Open access · greenAbstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
5.3field-weighted citation impact, top 5% 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

25 citing papers in PubMed, 47 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Lysophosphatidic acid induces tumor necrosis factor-alpha to regulate a pro-inflammatory cytokine network in ovarian cancer.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020
    Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Association of lipid metabolism with ovarian cancer.Current oncology (Toronto, Ont.) · 2010
    Article
  19. Article
  20. 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

10 authors at 1 institution in 1 country.

Regina A OyesanyaVirginia Commonwealth University, Department of Biochemistry and Molecular Biology, 1101 East Marshall St., Richmond, VA 23298, USA.
Zendra P Lee
Jinhua Wu
Jing Chen
Yuanda Song
Abir Mukherjee
Paul Dent
Tomasz Kordula
Huiping Zhou
Xianjun Fang
Virginia Commonwealth University · US

Funding

Virus Vector Shared ResourceP30CA016059 · NCI · VIRGINIA COMMONWEALTH UNIVERSITY · PI Keri R Maher · 1985 to 2026
$51.0M
Lysophospholipid in Neovascularization in Ovarian CancerR01CA102196 · NCI · VIRGINIA COMMONWEALTH UNIVERSITY · PI FANG, XIANJUN · 2004 to 2010
$1.4M
NCI NIH HHS CA102196NCI NIH HHS P30 CA016059NCI NIH HHS P30 CA16059NCI NIH HHS R01 CA102196
6 · The paper itself

Abstract

Emerging evidence suggests that lysophosphatidic acid (LPA) is a physiological regulator of cyclooxygenase-2 (Cox-2) expression. Herein we used ovarian cancer cells as a model to investigate the molecular mechanisms that link the LPA G protein-coupled receptors (GPCRs) to Cox-2 expression. LPA stimulated Cox-2 expression and release of prostaglandins though the LPA(1), LPA(2), and LPA(5) receptors. The effect of LPA involves both transcriptional activation and post-transcriptional enhancement of Cox-2 mRNA stability. The consensus sites for C/EBP in the Cox-2 promoter were essential for transcriptional activation of Cox-2 by LPA. The NF-kappaB and AP-1 transcription factors commonly involved in inducible Cox-2 expression were dispensable. Dominant-negative C/EPBbeta inhibited LPA activation of the Cox-2 promoter and expression. Furthermore, LPA stimulated C/EBPbeta phosphorylation and activity through a novel mechanism integrating GPCR signals and a permissive activity from a receptor tyrosine kinase (RTK). This role of RTK was not consistent with LPA activation of C/EBP through transactivation of RTK, as full activation of RTKs with their own agonists only weakly stimulated C/EBP. In addition to the transcriptional activation, the RNA stabilization protein HuR bound to and protected Cox-2 mRNA in LPA-stimulated cells, indicating an active role for HuR in sustaining Cox-2 induction during physiological responses.

Indexed as

Antigens, SurfaceArachidonic AcidBase SequenceCCAAT-Enhancer-Binding ProteinsCell Line, TumorCyclooxygenase 2DinoprostoneDNA PrimersELAV-Like Protein 1ELAV ProteinsFemaleHumansLysophospholipidsMutagenesis, Site-DirectedOvarian NeoplasmsPhosphorylationAntigens, SurfaceArachidonic AcidCCAAT-Enhancer-Binding ProteinsCyclooxygenase 2DinoprostoneDNA PrimersELAVL1 protein, humanELAV-Like Protein 1ELAV Proteinslysophosphatidic acidLysophospholipidsPTGS2 protein, humanReceptor Protein-Tyrosine KinasesReceptors, Lysophosphatidic AcidRNA-Binding ProteinsRNA, MessengerRNA, NeoplasmRNA, Small Interfering

Identifiers

PMID18362203
PMCPMC2493458
OpenAlexW2001052106

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.