Evidence map›Paper›PMID 15197583›Full record

ArticleJournal of cancer research and clinical oncology2004

Celecoxib induces apoptosis in cervical cancer cells independent of cyclooxygenase using NF-kappaB as a possible target.

Su-Hyeong Kim, Sang-Hyun Song, Sang-Gyun Kim, Kyung-Soo Chun, So-Young Lim, Hye-Kyung Na, Jae Weon Kim, Young-Joon Surh, Yung-Jue Bang, Yong-Sang Song

Open access · greenAbstract read
In one paragraph

Article in Journal of cancer research and clinical oncology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
6.4field-weighted citation impact, top 3% 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

25 citing papers in PubMed, 1 synthesis or guideline pooled it, 86 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. 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

10 authors at 2 institutions in 1 country.

Su-Hyeong KimCancer Research Institute, College of Medicine Seoul National University, Seoul, Korea.
Sang-Hyun Song
Sang-Gyun Kim
Kyung-Soo Chun
So-Young Lim
Hye-Kyung Na
Jae Weon Kim
Young-Joon Surh
Yung-Jue Bang
Yong-Sang Song
Seoul National University · KRSeoul National University Hospital · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeRecently, many studies have shown that celecoxib induces apoptosis in various cancer cells by different mechanisms depending on the cell type. This study examined the apoptotic effect of celecoxib in cervical cancer cells and its mechanism.

methodsCell viability was measured by MTT assay and apoptosis was examined by DNA fragmentation and flow cytometry. Western blotting and immunoprecipitation were used to explore various mechanisms of celecoxib-induced apoptosis. The activation of NF-kappaB was confirmed by EMSA.

resultsCelecoxib induced apoptosis independent of COX-2 activity. This event accompanied the activation of caspase-8 and -9 with Bid cleavage and the loss of mitochondrial membrane potential. The protective effect of caspase-8 and -9 inhibitors on celecoxib-induced apoptosis suggests the importance of caspase-8 and -9 activation in this apoptotic pathway. Fas/FADD-mediated apoptotic pathway was detected only in C33A cells, demonstrated by the immunoprecipitation of Fas-FADD in celecoxib-treated cells and the protective effect of FADD dominant negative mutant. Finally, NF-kappaB appeared to be involved in celecoxib-induced apoptosis, as revealed by increased NF-kB DNA binding activity in a time-dependent manner and attenuation of its proapoptotic effect by N-tosyl-L-phenylalanyl-chloromethyl ketone, an NF-kB blocker.

conclusionsThese data show that caspase-8 and -9 are involved in the apoptotic effect of celecoxib in cervical cancer cells. This requires the FADD-dependent pathway in a cell type-specific manner. In addition, NF-kappaB may play a key role in celecoxib-induced apoptosis.

Indexed as

Adaptor Proteins, Signal TransducingAntineoplastic AgentsApoptosisBlotting, WesternCaspasesCelecoxibCell Line, TumorCell ProliferationCyclooxygenase 2Cyclooxygenase 2 InhibitorsCyclooxygenase InhibitorsDNA FragmentationElectrophoretic Mobility Shift AssayFas-Associated Death Domain ProteinFemaleFlow CytometryAdaptor Proteins, Signal TransducingAntineoplastic AgentsCaspasesCelecoxibCyclooxygenase 2Cyclooxygenase 2 InhibitorsCyclooxygenase InhibitorsFADD protein, humanFas-Associated Death Domain ProteinIsoenzymesMembrane ProteinsNF-kappa BProstaglandin-Endoperoxide SynthasesPTGS2 protein, humanPyrazolesSulfonamides

Identifiers

PMID15197583
PMCPMC12161875
OpenAlexW1986936335

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.