Evidence map›Paper›PMID 21822307›Full record

ArticleOncogene2012

A common single-nucleotide polymorphism in cyclooxygenase-2 disrupts microRNA-mediated regulation.

A E Moore, L E Young, D A Dixon

Abstract read
In one paragraph

Article in Oncogene, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
4.1field-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

32 citing papers in PubMed, 55 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Reduction in gene expression noise by targeted increase in accessibility at gene loci.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Regulation of Eicosanoid Pathways by MicroRNAs.Frontiers in pharmacology · 2019
    Review
  15. Article
  16. Activated human T lymphocytes inhibit TGFβ-induced fibroblast to myofibroblast differentiation via prostaglandins DAmerican journal of physiology. Lung cellular and molecular physiology · 2018
    Article
  17. Modulation of the prostaglandin-endoperoxide synthase 2 gene expression by variant haplotypes: influence of the 3'-untranslated region.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2017
    Article
  18. Article
  19. Observational
  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

3 authors at 1 institution in 1 country.

A E MooreDepartment of Biological Sciences and Center for Colon Cancer Research, University of South Carolina, Columbia, SC 29208, USA.
L E Young
D A Dixon
University of South Carolina · US

Funding

Post-Transcriptional Regulation in Colorectal CancerR01CA134609 · NCI · UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA · PI DIXON, DAN ALAN · 2009 to 2013
$1.4M
NCI NIH HHS R01 CA134609NCI NIH HHS R01CA134609
6 · The paper itself

Abstract

Elevated expression of the prostaglandin synthase cyclooxygenase-2 (COX-2) is commonly observed in many chronic inflammatory diseases and cancer. However, the mechanisms allowing for pathogenic COX-2 overexpression are largely unknown. The gene for COX-2 (PTGS2) carries a common single-nucleotide polymorphism (SNP) at position 8473 (T8473C), in exon 10 that is associated with diseases in which COX-2 overexpression is a contributing factor. We demonstrate that the T8473C SNP resides within a region that targets COX-2 mRNA for degradation through microRNA-mediated regulation. miR-542-3p was identified to bind transcripts derived from the 8473T allele and promote mRNA decay. By contrast, the presence of the variant 8473C allele interfered with miR-542-3p binding, allowing for mRNA stabilization, and this effect was rescued using a mutated miR-542-3p at the respective 8473 site. Colon cancer cells and tissue displayed COX-2 mRNA levels that were dependent on T8473C allele dosage, and allele-specific expression of COX-2 was observed to be a contributing factor promoting COX-2 overexpression. These findings provide a novel molecular explanation underlying disease susceptibility associated with COX-2 T8473C SNP, and identify it as a potential marker for identifying cancer patients best served through selective COX-2 inhibition.

Indexed as

Gene Expression RegulationPolymorphism, Single NucleotideColonic NeoplasmsCyclooxygenase 2HumansMicroRNAsCyclooxygenase 2MicroRNAsMIRN542 microRNA, humanPTGS2 protein, human

Identifiers

PMID21822307
PMCPMC3454533
OpenAlexW2032267604

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.