Evidence map›Paper›PMID 14508518›Full record

ArticleOncogene2003

Early events in the induction of apoptosis in ovarian carcinoma cells by CD437: activation of the p38 MAP kinase signal pathway.

William F Holmes, Dianne Robert Soprano, Kenneth J Soprano

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

27 citing papers in PubMed, 75 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Targeting signaling pathways in epithelial ovarian cancer.International journal of molecular sciences · 2013
    Review
  15. Article
  16. Mitochondrial regulation of cell cycle and proliferation.Antioxidants & redox signaling · 2012
    Review
  17. Article
  18. Targeting NR4A1 (TR3) in cancer cells and tumors.Expert opinion on therapeutic targets · 2011
    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

3 authors at 1 institution in 1 country.

William F HolmesDepartment of Microbiology & Immunology, Temple University School of Medicine, 3400 North Broad Street, Philadelphia, PA 19140, USA.
Dianne Robert Soprano
Kenneth J Soprano
Temple University · US

Funding

TRAINING PROGRAMS IN MICROBIOLOGY &IMMUNOLOGYT32AI007101 · NIAID · TEMPLE UNIV OF THE COMMONWEALTH · PI GANEA, DOINA · 1985 to 2008
$2.4M
RETINOIDS FOR TREATMENT OF OVARIAN CARCINOMAR01CA064945 · NCI · TEMPLE UNIV OF THE COMMONWEALTH · PI SOPRANO, KENNETH J · 1994 to 2007
$1.9M
Mechanism of Retinoid Inhibition of Oral SCC Cell GrowthR01DE013139 · NIDCR · TEMPLE UNIVERSITY · PI SOPRANO, KENNETH J · 2001 to 2004
$837k
NCI NIH HHS CA 64945NIAID NIH HHS AI 07101NIDCR NIH HHS DE 13139
6 · The paper itself

Abstract

Retinoids have great potential in the areas of cancer therapy and chemoprevention. 6-[3-(1-admantyl)]-4-hydroxyphenyl]-2-naphthalene carboxylic acid (CD437) is a conformationally restricted synthetic retinoid that has been reported to induce growth arrest and apoptosis in ovarian tumor cell lines but the entire mechanism for apoptotic induction has not been fully defined. We set out to identify the early events of CD437-induced apoptosis of the CA-OV-3 cell line and determine if these occur in a CA-OV-3 cell line resistant to CD437 (CA-CD437R). Using inhibitors for the MAP kinase cascade, we determined that MEK and p38 inhibitors could block CD437-induced apoptosis of the CA-OV-3 cell line. Moreover, treatment of CA-OV-3 and CA-CD437R cells with CD437 resulted in increased phosphorylation and activity of p38 independent of caspase-3 activation. Furthermore, p38 induced the phosphorylation of MEF2 in both CA-OV-3 and CA-CD437R cells after CD437 treatment. Finally, GFP-TR3 protein translocated to the cytosol and associated with mitochondria in both cell lines in response to CD437 treatment. This leads to depolarization of mitochondria and subsequent induction of apoptosis only in CA-OV-3 cells. These results identify a number of initial molecular events in the induction of apoptosis by CD437 in CA-OV-3 cells and demonstrate that the alteration in CA-CD437R cells, which results in resistance to CD437 maps downstream of these early events after TR3 translocation but prior to mitochondrial depolarization.

Indexed as

MAP Kinase Kinase Kinase 1AnimalsAntineoplastic AgentsApoptosisCarcinomaEnzyme ActivationFemaleHumansMitogen-Activated Protein KinasesNuclear Receptor Subfamily 4, Group A, Member 1Ovarian Neoplasmsp38 Mitogen-Activated Protein KinasesProtein Serine-Threonine KinasesReceptors, SteroidReceptors, Thyroid HormoneRetinoidsAntineoplastic AgentsCD 437MAP3K1 protein, humanMAP Kinase Kinase Kinase 1Mitogen-Activated Protein KinasesNR4A1 protein, humanNuclear Receptor Subfamily 4, Group A, Member 1p38 Mitogen-Activated Protein KinasesProtein Serine-Threonine KinasesReceptors, SteroidReceptors, Thyroid HormoneRetinoids

Identifiers

PMID14508518
OpenAlexW1999284018

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.