Evidence map›Paper›PMID 16799641›Full record

ArticleOncogene2006

Detachment-induced upregulation of XIAP and cIAP2 delays anoikis of intestinal epithelial cells.

Z Liu, H Li, X Wu, B H Yoo, S R Yan, A W Stadnyk, T Sasazuki, S Shirasawa, E C LaCasse, R G Korneluk and 1 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2006. 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
2.0field-weighted citation impact, top 15% 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, 54 citations in OpenAlex.

  1. Review
  2. Article
  3. XIAP as a multifaceted molecule in Cellular Signaling.Apoptosis : an international journal on programmed cell death · 2022
    Review
  4. Article
  5. Article
  6. Molecularly-targeted therapy for the oral cancer stem cells.The Japanese dental science review · 2018
    Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. IGF1 stimulates crypt expansion via differential activation of 2 intestinal stem cell populations.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2015
    Article
  13. Regulation of anoikis by deleted in breast cancer-1 (DBC1) through NF-κB.Apoptosis : an international journal on programmed cell death · 2013
    Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  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

11 authors at 4 institutions in 2 countries.

Z LiuDepartment of Pediatrics, Atlantic Research Centre, Dalhousie University, Halifax, Nova Scotia, Canada.
H Li
X Wu
B H Yoo
S R Yan
A W Stadnyk
T Sasazuki
S Shirasawa
E C LaCasse
R G Korneluk
K V Rosen
Dalhousie University · CASaitama International Medical Center · JPChildren's Hospital of Eastern Ontario · CAUniversity of Ottawa · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Detachment of normal epithelial cells from the extracellular matrix triggers apoptosis, a phenomenon called anoikis. Conversely, carcinoma cells tend to be relatively more anoikis-resistant than their normal counterparts, and this increased resistance represents a critical feature of the malignant phenotype. Mechanisms that control susceptibility and resistance to anoikis are not fully understood. It is now known that detachment of non-malignant epithelial cells triggers both pro- and antiapoptotic signals, and it is the balance between these signals and the duration of detachment that determine further fate of the cells. Detachment-induced antiapoptotic events delay anoikis and if cells reattach relatively soon after detachment they survive. Direct regulators of apoptosis responsible for this delay of anoikis are unknown. We found that detachment of non-malignant intestinal epithelial cells triggers upregulation of inhibitors of apoptosis protein (IAP) family, such as X-chromosome-linked inhibitor of apoptosis protein and cellular inhibitor of apoptosis-2 (cIAP2). We demonstrated that this upregulation requires detachment-dependent activation of the transcription factor nuclear factor-kappaB. We further observed that various IAP antagonists accelerate anoikis, indicating that upregulation of the IAPs delays detachment-triggered apoptosis. We conclude that the IAPs are important regulators of the balance between detachment-triggered life and death signals. Perhaps, not by coincidence, these proteins are often upregulated in carcinomas, tumors composed of cells that tend to be anoikis-resistant.

Indexed as

AnoikisBaculoviral IAP Repeat-Containing 3 Proteinbcl-X ProteinCells, CulturedExtracellular MatrixHumansInhibitor of Apoptosis ProteinsIntestinal MucosaNF-kappa BUbiquitin-Protein LigasesUp-RegulationX-Linked Inhibitor of Apoptosis ProteinBaculoviral IAP Repeat-Containing 3 Proteinbcl-X ProteinBIRC3 protein, humanInhibitor of Apoptosis ProteinsNF-kappa BUbiquitin-Protein LigasesXIAP protein, humanX-Linked Inhibitor of Apoptosis Protein

Identifiers

PMID16799641
OpenAlexW1999895549

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.