Evidence map›Paper›PMID 17982483›Full record

ArticleOncogene2008

CK2 controls TRAIL and Fas sensitivity by regulating FLIP levels in endometrial carcinoma cells.

D Llobet, N Eritja, M Encinas, N Llecha, A Yeramian, J Pallares, A Sorolla, F J Gonzalez-Tallada, X Matias-Guiu, X Dolcet

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2008. 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
2.4field-weighted citation impact, top 11% 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, 54 citations in OpenAlex.

  1. Article
  2. Review
  3. Role of protein kinase CK2 in antitumor drug resistance.Journal of experimental & clinical cancer research : CR · 2019
    Review
  4. Article
  5. Article
  6. Article
  7. Luteolin induces apoptosis by activating Fas signaling pathway at the receptor level in laryngeal squamous cell line Hep-2 cells.European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery · 2014
    Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. DcR1 expression in endometrial carcinomas.Virchows Archiv : an international journal of pathology · 2010
    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 1 institution in 1 country.

D LlobetOncologic Pathology Group, Institut de Recerca Biomèdica de Lleida, IRBLleida, Lleida, Spain.
N Eritja
M Encinas
N Llecha
A Yeramian
J Pallares
A Sorolla
F J Gonzalez-Tallada
X Matias-Guiu
X Dolcet
Instituto de Investigación Biomédica de Lleida · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) has emerged as a promising antineoplastic agent because of its ability to selectively kill tumoral cells. However, some cancer cells are resistant to TRAIL-induced apoptosis. We have previously demonstrated that in endometrial carcinoma cells such resistance is caused by elevated FLICE-inhibitory protein (FLIP) levels. The present study focuses on the mechanisms by which FLIP could be modulated to sensitize endometrial carcinoma cells to TRAIL-induced apoptosis. We find that inhibition of casein kinase (CK2) sensitizes endometrial carcinoma cells to TRAIL- and Fas-induced apoptosis. CK2 inhibition correlates with a reduction of FLIP protein, suggesting that CK2 regulates resistance to TRAIL and Fas by controlling FLIP levels. FLIP downregulation correlates with a reduction of mRNA and is prevented by addition of the MG-132, suggesting that CK2 inhibition results in a proteasome-mediated degradation of FLIP. Consistently, forced expression of FLIP restores resistance to TRAIL and Fas. Moreover, knockdown of either FADD or caspase-8 abrogates apoptosis triggered by inhibition of CK2, indicating that CK2 sensitization requires formation of functional DISC. Finally, because of the possible role of both TRAIL and CK2 in cancer therapy, we demonstrate that CK2 inhibition sensitizes primary endometrial carcinoma explants to TRAIL apoptosis. In conclusion, we demonstrate that CK2 regulates endometrial carcinoma cell sensitivity to TRAIL and Fas by regulating FLIP levels.

Indexed as

Antineoplastic AgentsApoptosisCasein Kinase IICASP8 and FADD-Like Apoptosis Regulating ProteinCell LineDrug Resistance, NeoplasmEndometrial Neoplasmsfas ReceptorFemaleGene Expression Regulation, NeoplasticHumansLeupeptinsNeoplasm ProteinsProteasome Endopeptidase ComplexTNF-Related Apoptosis-Inducing LigandTumor Cells, CulturedAntineoplastic Agentsbenzyloxycarbonylleucyl-leucyl-leucine aldehydeCasein Kinase IICASP8 and FADD-Like Apoptosis Regulating Proteinfas ReceptorLeupeptinsNeoplasm ProteinsProteasome Endopeptidase ComplexTNF-Related Apoptosis-Inducing LigandTNFSF10 protein, human

Identifiers

PMID17982483
OpenAlexW2033354569

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.