Evidence map›Paper›PMID 16168112›Full record

ArticleBreast cancer research : BCR2005

Epigenetic silencing of DSC3 is a common event in human breast cancer.

Marc M Oshiro, Christina J Kim, Ryan J Wozniak, Damian J Junk, José L Muñoz-Rodríguez, Jeanne A Burr, Matthew Fitzgerald, Sangita C Pawar, Anne E Cress, Frederick E Domann and 1 more

Open access · goldAbstract read
In one paragraph

Article in Breast cancer research : BCR, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed, 1 pooled it
2.6field-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

56 citing papers in PubMed, 1 synthesis or guideline pooled it, 114 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Article
  5. Article
  6. Article
  7. Expression and associated epigenetic mechanisms of the CaJournal of cell communication and signaling · 2022
    Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Epigenetic basis of cancer health disparities: Looking beyond genetic differences.Biochimica et biophysica acta. Reviews on cancer · 2017
    Review
  18. The role of desmosomes in carcinogenesis.OncoTargets and therapy · 2017
    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

11 authors at 2 institutions in 1 country.

Marc M OshiroDepartment of Pharmacology, Arizona Cancer Center, University of Arizona, Tucson, AZ, USA. moshiro@azcc.arizona.edu
Christina J Kim
Ryan J Wozniak
Damian J Junk
José L Muñoz-Rodríguez
Jeanne A Burr
Matthew Fitzgerald
Sangita C Pawar
Anne E Cress
Frederick E Domann
Bernard W Futscher
University of Arizona · USUniversity of Iowa · US

Funding

VITAMIN AP30CA023074 · NCI · UNIVERSITY OF ARIZONA · PI Dan Theodorescu · 1985 to 2026
$110.2M
Training in Environmental Toxicology of Human DiseaseT32ES007091 · NIEHS · UNIVERSITY OF ARIZONA · PI Nathan J Cherrington · 1985 to 2026
$10.7M
Integrative Cancer Scholars Training GrantT32CA009213 · NCI · UNIVERSITY OF ARIZONA · PI CAREW, JENNIFER S, CURIEL-LEWANDROWSKI, CLARA · 1985 to 2024
$8.6M
ROLE OF METALLOPROTEINASES AND TIMP IN HUMAN PROSTATE CELL INVASIONP01CA056666 · NCI · UNIVERSITY OF ARIZONA · PI HEIMARK, RONALD L. · 1993 to 2008
$6.3M
Genomic Methylation--Mechanism to Alter Tumor PhenotypesR01CA065662 · NCI · UNIVERSITY OF ARIZONA · PI FUTSCHER, BERNARD W · 2001 to 2009
$2.3M
RADIATION SIGNALING THROUGH THE ALPHA6 BETA4 INTEGRINR01CA075152 · NCI · UNIVERSITY OF ARIZONA · PI CRESS, ANNE ELIZABETH · 1998 to 2005
$1.5M
Epigenetic factors governing SOD2 gene expressionR01CA073612 · NCI · UNIVERSITY OF IOWA · PI DOMANN, FREDERICK E · 2003 to 2007
$1.3M
DNA METHYLATION AND SOD2/MNSOD GENE EXPRESSIONR29CA073612 · NCI · UNIVERSITY OF IOWA · PI DOMANN, FREDERICK E · 1998 to 2002
$321k
Chromatin Remodeling and SOD2 Expression in CancerR56CA073612 · NCI · UNIVERSITY OF IOWA · PI DOMANN, FREDERICK E · 2009 to 2009
$266k
GENOMIC METHYLATION--A MECHANISM TO ALTER PHENOTYPESR29CA065662 · NCI · UNIVERSITY OF ARIZONA · PI FUTSCHER, BERNARD W · 1996 to 2000
$106k
NCI NIH HHS CA56666NCI NIH HHS CA65662NCI NIH HHS CA73612NCI NIH HHS CA75152NCI NIH HHS P01 CA056666NCI NIH HHS P30 CA023074NCI NIH HHS P30 CA23074NCI NIH HHS R01 CA065662NCI NIH HHS R01 CA073612NCI NIH HHS R01 CA075152NCI NIH HHS R29 CA065662NCI NIH HHS R29 CA073612NCI NIH HHS R56 CA073612NCI NIH HHS T32 CA009213NCI NIH HHS T32 CA09213NIEHS NIH HHS ES07091NIEHS NIH HHS T32 ES007091
6 · The paper itself

Abstract

introductionDesmocollin 3 (DSC3) is a member of the cadherin superfamily of calcium-dependent cell adhesion molecules and a principle component of desmosomes. Desmosomal proteins such as DSC3 are integral to the maintenance of tissue architecture and the loss of these components leads to a lack of adhesion and a gain of cellular mobility. DSC3 expression is down-regulated in breast cancer cell lines and primary breast tumors; however, the loss of DSC3 is not due to gene deletion or gross rearrangement of the gene. In this study, we examined the prevalence of epigenetic silencing of DSC3 gene expression in primary breast tumor specimens.

methodsWe used bisulfite genomic sequencing to analyze the methylation state of the DSC3 promoter region from 32 primary breast tumor specimens. We also used a quantitative real-time RT-PCR approach, and analyzed all breast tumor specimens for DSC3 expression. Finally, in addition to bisulfite sequencing and RT-PCR, we used an in vivo nuclease accessibility assay to determine the chromatin architecture of the CpG island region from DSC3-negative breast cancer cells lines.

resultsDSC3 expression was downregulated in 23 of 32 (72%) breast cancer specimens comprising: 22 invasive ductal carcinomas, 7 invasive lobular breast carcinomas, 2 invasive ductal carcinomas that metastasized to the lymph node, and a mucoid ductal carcinoma. Of the 23 specimens showing a loss of DSC3 expression, 13 (56%) were associated with cytosine hypermethylation of the promoter region. Furthermore, DSC3 expression is limited to cells of epithelial origin and its expression of mRNA and protein is lost in a high proportion of breast tumor cell lines (79%). Lastly, DNA hypermethylation of the DSC3 promoter is highly correlated with a closed chromatin structure.

conclusionThese results indicate that the loss of DSC3 expression is a common event in primary breast tumor specimens, and that DSC3 gene silencing in breast tumors is frequently linked to aberrant cytosine methylation and concomitant changes in chromatin structure.

Indexed as

Gene SilencingBreast NeoplasmsDesmocollinsDNA MethylationDNA PrimersEpithelial CellsFemaleHumansMaleMastectomyMastectomy, SegmentalMembrane GlycoproteinsPromoter Regions, GeneticProstateRNA, NeoplasmDesmocollinsDNA PrimersDSC3 protein, humanMembrane GlycoproteinsRNA, Neoplasm

Identifiers

PMID16168112
PMCPMC1242132
OpenAlexW1532318361

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.