Evidence map›Paper›PMID 18648368›Full record

ArticleBritish journal of cancer2008

Prostaglandin E2 stimulates Fas ligand expression via the EP1 receptor in colon cancer cells.

G O'Callaghan, J Kelly, F Shanahan, A Houston

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
4.0field-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

20 citing papers in PubMed, 38 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. EP1 receptor is involved in prostaglandin E2-induced osteosarcoma growth.Bosnian journal of basic medical sciences · 2019
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Retinoic acid morpholine amide (RAMA) inhibits expression of Fas ligand through EP1 receptor in colon cancer cells.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
  11. Review
  12. Article
  13. Probiotics for the treatment of Clostridium difficile associated disease.World journal of gastrointestinal pathophysiology · 2013
    Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. The tumor microenvironment in colorectal carcinogenesis.Cancer microenvironment : official journal of the International Cancer Microenvironment Society · 2010
    Article
  20. Article
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.

G O'CallaghanDepartment of Medicine, University College Cork, National University of Ireland, Clinical Science Building, Cork University Hospital, Wilton, Cork, Ireland.
J Kelly
F Shanahan
A Houston
National University of Ireland · IEUniversity College Cork · IE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fas ligand (FasL/CD95L) is a member of the tumour necrosis factor superfamily that triggers apoptosis following crosslinking of the Fas receptor. Despite studies strongly implicating tumour-expressed FasL as a major inhibitor of the anti-tumour immune response, little is known about the mechanisms that regulate FasL expression in tumours. In this study, we show that the cyclooxygenase (COX) signalling pathway, and in particular prostaglandin E(2) (PGE(2)), plays a role in the upregulation of FasL expression in colon cancer. Suppression of either COX-2 or COX-1 by RNA interference in HCA-7 and HT29 colon tumour cells reduced FasL expression at both the mRNA and protein level. Conversely, stimulation with PGE(2) increased FasL expression and these cells showed increased cytotoxicity against Fas-sensitive Jurkat T cells. Prostaglandin E(2)-induced FasL expression was mediated by signalling via the EP1 receptor. Moreover, immunohistochemical analysis using serial sections of human colon adenocarcinomas revealed a strong positive correlation between COX-2 and FasL (r=0.722; P<0.0001) expression, and between EP1 receptor and FasL (r=0.740; P<0.0001) expression, in the tumour cells. Thus, these findings indicate that PGE(2) positively regulates FasL expression in colon tumour cells, adding another pro-neoplastic activity to PGE(2).

Indexed as

Blotting, WesternCell Line, TumorCoculture TechniquesColonic NeoplasmsDinoprostoneEnzyme-Linked Immunosorbent AssayFas Ligand ProteinFluorescent Antibody TechniqueHumansReceptors, Prostaglandin EReceptors, Prostaglandin E, EP1 SubtypeRNA InterferenceRNA, MessengerSignal TransductionDinoprostoneFas Ligand ProteinPTGER1 protein, humanReceptors, Prostaglandin EReceptors, Prostaglandin E, EP1 SubtypeRNA, Messenger

Identifiers

PMID18648368
PMCPMC2527805
OpenAlexW1976875629

What OpenQuestion holds

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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.