Evidence map›Paper›PMID 12370831›Full record

ArticleOncogene2002

The role of p38 in UVA-induced cyclooxygenase-2 expression in the human keratinocyte cell line, HaCaT.

Michael A Bachelor, Amy L Silvers, Gim T Bowden

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
3.7field-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

17 citing papers in PubMed, 66 citations in OpenAlex.

  1. Trial
  2. Protective effects of Oroxylum indicum seed extract against ultraviolet-induced skin photodamage through inhibition of STING and NF-κB signaling pathways.Photochemical & photobiological sciences : Official journal of the European Photochemistry Association and the European Society for Photobiology · 2026
    Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Autophagy in UV Damage Response.Photochemistry and photobiology · 2017
    Review
  8. Article
  9. Activation of p38 MAP kinase and JNK pathways by UVA irradiation.Photochemical & photobiological sciences : Official journal of the European Photochemistry Association and the European Society for Photobiology · 2012
    Article
  10. Article
  11. Article
  12. Article
  13. Article
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  15. 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.

Michael A BachelorDepartment of Radiation Oncology, Arizona Cancer Center, The University of Arizona, 1515 North Campbell Avenue, Tucson 85724, USA.
Amy L Silvers
Gim T Bowden
University of Arizona · US

Funding

VITAMIN AP30CA023074 · NCI · UNIVERSITY OF ARIZONA · PI Dan Theodorescu · 1985 to 2026
$110.2M
VITAMIN A, AND ITS PRECURSORS AND DERIVATIVES AS THERAPEUTIC MODALITIESP01CA027502 · NCI · UNIVERSITY OF ARIZONA · PI EINSPAHR, JANINE G · 1985 to 2015
$36.3M
NCI NIH HHS CA23074NCI NIH HHS CA27502
6 · The paper itself

Abstract

We examined the expression of cycloxygenase-2, the rate-limiting enzyme in the production of prostaglandins, in the UVA-irradiated human keratinocyte cell line, HaCaT. UVA induced a dose-dependent increase in COX-2 at the protein level at 2 and 4 h post-irradiation and at the mRNA level at 1 and 2 h post-irradiation. Experiments using semi-quantitative RT-PCR demonstrate that UVA increased the half-life of the COX-2 message by more than fourfold in the presence of Actinomycin D (with a half life between 4 and 8 h post-irradiation), suggesting that UVA induction of COX-2 is post-transcriptionally regulated. Through the use of the specific p38 inhibitor, SB202190, increases in COX-2 message and protein levels were abrogated in UVA-irradiated cells. In UVA-irradiated cells treated with SB202190, the half-life of the COX-2 message was decreased to basal levels (between 1 and 2 h post-irradiation), indicating that p38 was responsible for the stabilization of the message. Luciferase activity was increased in UVA-irradiated cells transfected with reporter constructs containing the 3' UTR of COX-2, a region containing AU-rich elements (AREs). These regulatory sequences of AUUUA have been proposed as one mechanism of post-transcriptional regulation. Increases observed in luciferase activity could be decreased using a p38 dominant-negative construct. We report for the first that UVA can induce COX-2 expression in the human keratinocyte cell line, HaCaT. Additionally, p38 appears to play a critical role in the UVA-induced expression of COX-2 in these keratinocytes and may serve as a potential drug target in the chemoprevention of skin cancer.

Indexed as

Ultraviolet Rays3' Untranslated RegionsCell LineCyclooxygenase 2Cyclooxygenase 2 InhibitorsCyclooxygenase InhibitorsHumansImidazolesIsoenzymesKeratinocytesMembrane ProteinsMitogen-Activated Protein Kinasesp38 Mitogen-Activated Protein KinasesProstaglandin-Endoperoxide SynthasesPyridinesRNA, Messenger3' Untranslated Regions4-(4-fluorophenyl)-2-(4-hydroxyphenyl)-5-(4-pyridyl)imidazoleCyclooxygenase 2Cyclooxygenase 2 InhibitorsCyclooxygenase InhibitorsImidazolesIsoenzymesMembrane ProteinsMitogen-Activated Protein Kinasesp38 Mitogen-Activated Protein KinasesProstaglandin-Endoperoxide SynthasesPTGS2 protein, humanPyridinesRNA, Messenger

Identifiers

PMID12370831
OpenAlexW1999997271

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.