Evidence map›Paper›PMID 15688023›Full record

ArticleOncogene2005

Casein kinase II (CK2) enhances death-inducing signaling complex (DISC) activity in TRAIL-induced apoptosis in human colon carcinoma cell lines.

Kamel Izeradjene, Leslie Douglas, Addison Delaney, Janet A Houghton

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

35 citing papers in PubMed, 87 citations in OpenAlex.

  1. Article
  2. Pro-Apoptotic Activity of 1-(4,5,6,7-Tetrabromo-1International journal of molecular sciences · 2025
    Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Synthesis of Novel Acyl Derivatives of 3-(4,5,6,7-Tetrabromo-1International journal of molecular sciences · 2021
    Article
  9. Review
  10. Article
  11. Protein Kinase CK2, a Potential Therapeutic Target in Carcinoma ManagementAsian Pacific journal of cancer prevention : APJCP · 2019
    Review
  12. Article
  13. Article
  14. Review
  15. Review
  16. Review
  17. Review
  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

4 authors at 1 institution in 1 country.

Kamel IzeradjeneDivision of Molecular Therapeutics, Department of Hematology-Oncology, St Jude Children's Research Hospital, 332 North Lauderdale, Memphis, TN 38105, USA. kamel.izeradjene@stjude.org
Leslie Douglas
Addison Delaney
Janet A Houghton
St. Jude Children's Research Hospital · US

Funding

Viral Vector Technology (VVTSR)P30CA021765 · NCI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI CHARLES ROBERTS · 1985 to 2026
$166.9M
SELECTIVE THERAPY FOR COLON CARCINOMAR01CA032613 · NCI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI HOUGHTON, JANET ANNE · 1985 to 2007
$2.4M
SELECTIVE THERAPY FOR COLON CARCINOMAR37CA032613 · NCI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI HOUGHTON, JANET ANNE · 1994 to 1998
–
NCI NIH HHS CA 21765NCI NIH HHS CA 32613
6 · The paper itself

Abstract

Protein kinase casein kinase II (CK2) is increased in response to diverse growth stimuli, as well as being elevated in many human cancers examined. We have demonstrated that CK2 is a key survival factor that protects human colon carcinoma cells from TNF-related apoptosis-inducing ligand (TRAIL)-induced apoptosis. We determined that inhibition of CK2 phosphorylation events by DRB (5,6-dichlorobenzimidazole) resulted in dramatic sensitization of tumor cells to TRAIL-induced apoptosis, in the absence of effects in normal cells. Sensitization was caspase dependent, and independent of regulation via NF-kappaB. Further, inhibition of phosphorylation by CK2 did not modify the expression level of antiapoptotic proteins. Analysis of TRAIL-induced death-inducing signaling complex (DISC) formation demonstrated enhanced formation of the DISC, enhanced cleavage of caspase-8 and cleavage of Bid in the presence of DRB, thereby facilitating the release of proapoptotic factors from the mitochondria with subsequent downregulation of the expression of XIAP and c-IAP1. Further, silencing of CK2alpha in HT29 cells following transfection of CK2alpha shRNA abrogated CK2 kinase activity while simultaneously increasing TRAIL sensitivity. These findings demonstrate that CK2 plays a critical antiapoptotic role by conferring resistance to TRAIL at the level of the DISC.

Indexed as

AdenocarcinomaApigeninApoptosisApoptosis Regulatory ProteinsCasein Kinase IICell DeathCell Line, TumorColonic NeoplasmsDeath Domain Receptor Signaling Adaptor ProteinsEnzyme InhibitorsGenetic VectorsHumansIndolesKineticsMaleimidesMembrane GlycoproteinsApigeninApoptosis Regulatory ProteinsbisindolylmaleimideCasein Kinase IIDeath Domain Receptor Signaling Adaptor ProteinsEnzyme InhibitorsIndolesMaleimidesMembrane GlycoproteinsReceptors, Tumor Necrosis FactorRecombinant ProteinsTNF-Related Apoptosis-Inducing LigandTNFSF10 protein, humanTumor Necrosis Factor-alpha

Identifiers

PMID15688023
OpenAlexW1981619037

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.