Evidence map›Paper›PMID 20887552›Full record

ArticleCell proliferation2010

The role of inhibitor of DNA-binding (Id1) in hyperproliferation of keratinocytes: the pathological basis for middle ear cholesteatoma from chronic otitis media.

Y Hamajima, M Komori, D A Preciado, D I Choo, K Moribe, S Murakami, F G Ondrey, J Lin

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell proliferation, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
0.8field-weighted citation impact, top 24% 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

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Morphopathogenesis of Adult Acquired Cholesteatoma.Medicina (Kaunas, Lithuania) · 2023
    Article
  10. Article
  11. Review of potential medical treatments for middle ear cholesteatoma.Cell communication and signaling : CCS · 2022
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. The role of bone resorption in the etiopathogenesis of acquired middle ear cholesteatoma.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 · 2017
    Review
  18. Review
  19. Article
  20. Panel 4: Recent advances in otitis media in molecular biology, biochemistry, genetics, and animal models.Otolaryngology--head and neck surgery : official journal of American Academy of Otolaryngology-Head and Neck Surgery · 2013
    Review
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

8 authors at 3 institutions in 2 countries.

Y HamajimaDepartment of Otolaryngology-Head and Neck Surgery, University of Minnesota, Minneapolis, MN 55455, USA.
M Komori
D A Preciado
D I Choo
K Moribe
S Murakami
F G Ondrey
J Lin
University of Minnesota · USNagoya City University · JPCincinnati Children's Hospital Medical Center · US

Funding

Mucous cell metaplasia in pneumococcal otitis mediaR01DC008165 · NIDCD · UNIVERSITY OF MINNESOTA · PI LIN, JIZHEN · 2007 to 2011
$1.7M
Mutation of the Id1 gene in squamous cell cancerR03CA107989 · NCI · UNIVERSITY OF MINNESOTA TWIN CITIES · PI LIN, JIZHEN · 2004 to 2005
$149k
NCI NIH HHS R03 CA107989NIDCD NIH HHS R01 DC008165PHS HHS R01 00010055
6 · The paper itself

Abstract

objectivesA hallmark of cholesteatoma is hyperproliferation of keratinocytes with abundant production of keratins in the middle ear under chronic inflammatory conditions. However, little is known about the driving force of cellular proliferation and keratin production of cholesteatomal matrix. The purpose of this study was to investigate the cellular proliferation and keratin production of keratinocytes under the influence of Id1, a candidate transcription factor to cell proliferation. MATERIALS AND

methodsKeratinocytes were transfected with Id1 and the responses of keratinocytes to Id1 were studied by using cellular and molecular biologic methods.

resultsId1 positively contributed to the cell cycle progression and negatively to the p16(Ink4a) downregulation via the nuclear factor-kappa B (NF-κB)/cyclin D1 pathway. Id1 significantly increased the promoter activity of NF-κB which, in turn, up-regulated the expression of cyclin D1 and keratin 10 in keratinocytes. Specific NF-κB inhibitors (pyrrolidine dithiocarbamate, PDTC), or dominant-negative inhibitor (I kappa B alpha mutant, IκBαM) abrogated the Id1-induced cell proliferation and keratin 10 production whereas p65, a subunit of the NF-κB heterodimer and an enhancer of the NF-κB activity, strengthened the Id1-induced cell proliferation and keratin 10 production.

conclusionsId1 contributed to hyperproliferation of keratinocytes via enhancement of cell cycle progression, removal of cell cycle inhibition, and simultaneously increased keratin production.

Indexed as

Cell ProliferationCell LineCholesteatoma, Middle EarCyclin D1Cyclin-Dependent Kinase Inhibitor p16Down-RegulationHumansInhibitor of Differentiation Protein 1Keratin-10KeratinocytesKi-67 AntigenNF-kappa BOtitis MediaTransfectionUp-RegulationCyclin D1Cyclin-Dependent Kinase Inhibitor p16ID1 protein, humanInhibitor of Differentiation Protein 1Keratin-10Ki-67 AntigenNF-kappa B

Identifiers

PMID20887552
PMCPMC2950310
OpenAlexW1584737256

What OpenQuestion holds

Textmetadata
LicenceTDM
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.