Evidence map›Paper›PMID 19139136›Full record

ArticleMolecular cancer therapeutics2009

NS-398, ibuprofen, and cyclooxygenase-2 RNA interference produce significantly different gene expression profiles in prostate cancer cells.

Molykutty John-Aryankalayil, Sanjeewani T Palayoor, David Cerna, Michael T Falduto, Scott R Magnuson, C Norman Coleman

Open access · bronzeAbstract read
In one paragraph

Article in Molecular cancer therapeutics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
4.3field-weighted citation impact, top 6% 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

23 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
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  3. Emerging evidence for adapting radiotherapy to immunotherapy.Nature reviews. Clinical oncology · 2023
    Review
  4. Article
  5. Radiation-induced Adaptive Response: New Potential for Cancer Treatment.Clinical cancer research : an official journal of the American Association for Cancer Research · 2020
    Review
  6. Anti-Inflammatory Drug Use and Ovarian Cancer Risk by COX1/COX2 Expression and Infiltration of Tumor-Associated Macrophages.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2018
    Article
  7. Article
  8. Article
  9. Improving the Predictive Value of Preclinical Studies in Support of Radiotherapy Clinical Trials.Clinical cancer research : an official journal of the American Association for Cancer Research · 2016
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
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  19. 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

6 authors at 3 institutions in 1 country.

Molykutty John-AryankalayilRadiation Oncology Branch, Center for Cancer Research, National Cancer Institute, NIH, 9000 Rockville Pike, Room B3 B 406, Building 10, Bethesda, MD 20892, USA. Aryankalayilm@mail.nih.gov
Sanjeewani T Palayoor
David Cerna
Michael T Falduto
Scott R Magnuson
C Norman Coleman
National Cancer Institute · USGenUs BioSystems (United States) · USCenter for Cancer Research · US

Funding

Intramural NIH HHS Z99 CA999999
6 · The paper itself

Abstract

Cyclooxygenase-2 (COX-2) plays a significant role in tumor development and progression. Nonsteroidal anti-inflammatory drugs (NSAID) exhibit potent anticancer effects in vitro and in vivo by COX-2-dependent and COX-2-independent mechanisms. In this study, we used microarray analysis to identify the change of expression profile regulated by a COX-2-specific NSAID NS-398 (0.01 and 0.1 mmol/L), a nonspecific NSAID ibuprofen (0.1 and 1.5 mmol/L) and RNA interference (RNAi)-mediated COX-2 inhibition in PC3 prostate cancer cells. A total of 3,362 differentially expressed genes with 2-fold change and P<0.05 were identified. Low concentrations of NSAIDs and COX-2 RNAi altered very few genes (1-3%) compared with the higher concentration of NS-398 (17%) and ibuprofen (80%). Ingenuity Pathway Analysis was used for distributing the differentially expressed genes into biological networks and for evaluation of functional significance. The top 3 networks for both NSAIDs included functional categories of DNA replication, recombination and repair, and gastrointestinal disease. Immunoresponse function was specific to NS-398, and cell cycle and cellular movement were among the top functions for ibuprofen. Ingenuity Pathway Analysis also identified renal and urologic disease as a function specific for ibuprofen. This comprehensive study identified several COX-2-independent targets of NSAIDs, which may help explain the antitumor and radiosensitizing effects of NSAIDs. However, none of these categories were reflected in the identified networks in PC3 cells treated with clinically relevant low concentrations of NS-398 and ibuprofen or with COX-2 RNAi, suggesting the benefit to fingerprinting preclinical drug concentrations to improve their relevance to the clinical setting.

Indexed as

RNA InterferenceAngiopoietin-Like Protein 4AngiopoietinsAnti-Inflammatory Agents, Non-SteroidalCell Line, TumorCell SurvivalCyclooxygenase 2Cyclooxygenase 2 InhibitorsGene Expression ProfilingGene Expression Regulation, NeoplasticGene Knockdown TechniquesHot TemperatureHumansIbuprofenMaleMatrix Metalloproteinase 3Angiopoietin-Like Protein 4AngiopoietinsANGPTL4 protein, humanAnti-Inflammatory Agents, Non-SteroidalCyclooxygenase 2Cyclooxygenase 2 InhibitorsIbuprofenMatrix Metalloproteinase 3N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamideNitrobenzenesPTGS2 protein, humanSulfonamides

Identifiers

PMID19139136
PMCPMC2861287
OpenAlexW2097649317

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.