Evidence map›Paper›PMID 21681825›Full record

ArticleMolecular carcinogenesis2012

Loss of Desmocollin 3 in skin tumor development and progression.

Jiangli Chen, Charlene O'Shea, James E Fitzpatrick, Maranke I Koster, Peter J Koch

Open access · greenAbstract read
In one paragraph

Article in Molecular carcinogenesis, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.1field-weighted citation impact, top 25% 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

14 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Article
  3. Desmosomal Cadherins in Health and Disease.Annual review of pathology · 2022
    Review
  4. Review
  5. Article
  6. The role of desmosomes in carcinogenesis.OncoTargets and therapy · 2017
    Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Plakoglobin as a regulator of desmocollin gene expression.The Journal of investigative dermatology · 2013
    Article
  13. Article
  14. 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

5 authors at 2 institutions in 1 country.

Jiangli ChenDepartment of Dermatology, University of Colorado Denver, Aurora, CO 80045, USA.
Charlene O'Shea
James E Fitzpatrick
Maranke I Koster
Peter J Koch
University of Colorado Denver · USGates (United States) · US

Funding

Colorado Clinical and Translational Sciences InstituteUL1TR001082 · NCATS · UNIVERSITY OF COLORADO DENVER · PI SOKOL, RONALD J. · 2013 to 2017
$48.0M
Cross-talk Between Desmosomal Proteins and Signaling Pathways in the SkinR01AR053892 · NIAMS · UNIVERSITY OF COLORADO DENVER · PI KOCH, PETER J. · 2008 to 2012
$1.9M
Desmocollin 3 in the development and maintenance tissuesR01AR050439 · NIAMS · UNIVERSITY OF COLORADO DENVER · PI KOCH, PETER J. · 2004 to 2008
$1.5M
NCATS NIH HHS UL1 TR001082NIAMS NIH HHS R01 AR050439NIAMS NIH HHS R01 AR053892
6 · The paper itself

Abstract

Desmocollin 3 (DSC3) is a desmosomal cadherin that is required for maintaining cell adhesion in the epidermis as demonstrated by the intra-epidermal blistering observed in Dsc3 null skin. Recently, it has been suggested that deregulated expression of DSC3 occurs in certain human tumor types. It is not clear whether DSC3 plays a role in the development or progression of cancers arising in stratified epithelia such as the epidermis. To address this issue, we generated a mouse model in which Dsc3 expression is ablated in K-Ras oncogene-induced skin tumors. Our results demonstrate that loss of Dsc3 leads to an increase in K-Ras-induced skin tumors. We hypothesize that acantholysis-induced epidermal hyperplasia in the Dsc3 null epidermis facilitates Ras-induced tumor development. Further, we demonstrate that spontaneous loss of DSC3 expression is a common occurrence during human and mouse skin tumor progression. This loss occurs in tumor cells invading the dermis. Interestingly, other desmosomal proteins are still expressed in tumor cells that lack DSC3, suggesting a specific function of DSC3 loss in tumor progression. While loss of DSC3 on the skin surface leads to epidermal blistering, it does not appear to induce loss of cell-cell adhesion in tumor cells invading the dermis, most likely due to a protection of these cells within the dermis from mechanical stress. We thus hypothesize that DSC3 can contribute to the progression of tumors both by cell adhesion-dependent (skin surface) and likely by cell adhesion-independent (invading tumor cells) mechanisms.

Indexed as

AllelesAnimalsBiomarkers, TumorCarcinoma, Squamous CellDesmocollinsDisease ProgressionGenes, rasHumansMembrane GlycoproteinsMiceSkin NeoplasmsBiomarkers, TumorDesmocollinsDsc3 protein, mouseMembrane Glycoproteins

Identifiers

PMID21681825
PMCPMC3178010
OpenAlexW2082715573

What OpenQuestion holds

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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.