Evidence map›Paper›PMID 11815387›Full record

ArticleBritish journal of pharmacology2002

Different glucocorticoids vary in their genomic and non-genomic mechanism of action in A549 cells.

Jamie D Croxtall, Peter Th W van Hal, Qam Choudhury, Derek W Gilroy, Rod J Flower

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in British journal of pharmacology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed, 2 pooled it
4.7field-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

45 citing papers in PubMed, 2 syntheses or guidelines pooled it, 146 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Review
  5. Article
  6. The Role of Glucocorticoids in Breast Cancer Therapy.Current oncology (Toronto, Ont.) · 2022
    Review
  7. Review
  8. Article
  9. Review
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  11. Article
  12. Article
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  16. Article
  17. Understanding how long-acting βBritish journal of pharmacology · 2016
    Review
  18. 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

5 authors at 3 institutions in 2 countries.

Jamie D CroxtallDepartment of Biochemical Pharmacology, The William Harvey Research Institute, St. Bartholomew's and the Royal London School of Medicine & Dentistry (Queen Mary and Westfield College), Charterhouse Square, London EC1M 6BQ. J.Croxtall@qmul.ac.uk
Peter Th W van Hal
Qam Choudhury
Derek W Gilroy
Rod J Flower
Queen Mary University of London · GBRotterdam University of Applied Sciences · NLWilliam Harvey Research Institute · GB

Funding

Wellcome Trust
6 · The paper itself

Abstract

We have examined the effects of 12 glucocorticoids as inhibitors of A549 cell growth. Other than cortisone and prednisone, all the glucocorticoids inhibited cell growth and this was strongly correlated (r=0.91) with inhibition of prostaglandin (PG)E(2) formation. The molecular mechanism by which the active steroids prevented PGE(2) synthesis was examined and three groups were identified. Group A drugs did not inhibit arachidonic acid release but inhibited the induction of COX2. Group B drugs were not able to inhibit the induction of COX2 but inhibited arachidonic acid release through suppression of cPLA(2) activation. Group C drugs were apparently able to bring about both effects. The inhibitory actions of all steroids was dependent upon glucocorticoid receptor occupation since RU486 reversed their effects. However, group A acted through the NF-kappaB pathway to inhibit COX2 as the response was blocked by the inhibitor geldanamycin which prevents dissociation of GR and the effect was blocked by APDC, the NF-kappaB inhibitor. On the other hand, the group B drugs were not inhibited by NF-kappaB inhibitors or geldanamycin but their effect was abolished by the src inhibitor PP2. Group C drugs depended on both pathways. In terms of PGE(2) generation, there is clear evidence of two entirely separate mechanisms of glucocorticoid action, one of which correlates with NF-kappaB mediated genomic actions whilst the other, depends upon rapid effects on a cell signalling system which does not require dissociation of GR. The implications for these findings are discussed.

Indexed as

Arachidonic AcidCell DivisionCyclooxygenase 2DexamethasoneDinoprostoneEnzyme ActivationGene Expression Regulation, EnzymologicGlucocorticoidsHumansIsoenzymesMembrane ProteinsPhospholipases AProstaglandin-Endoperoxide SynthasesSignal TransductionTumor Cells, CulturedArachidonic AcidCyclooxygenase 2DexamethasoneDinoprostoneGlucocorticoidsIsoenzymesMembrane ProteinsPhospholipases AProstaglandin-Endoperoxide SynthasesPTGS2 protein, human

Identifiers

PMID11815387
PMCPMC1573139
OpenAlexW2040291484

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.