Evidence map›Paper›PMID 19141643›Full record

ArticleCancer research2009

Transcriptional repression of epithelial cell adhesion molecule contributes to p53 control of breast cancer invasion.

Narendra V Sankpal, Michael W Willman, Timothy P Fleming, John D Mayfield, William E Gillanders

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed, 1 pooled it
4.1field-weighted citation impact, top 5% 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

58 citing papers in PubMed, 1 synthesis or guideline pooled it, 89 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Emerging roles of aerobic glycolysis in breast cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2020
    Review
  12. Shedding light on the EpCAM: An overview.Journal of cellular physiology · 2019
    Review
  13. Review
  14. Article
  15. Article
  16. A New in Vitro Model of GDLD by Knocking OutTranslational vision science & technology · 2018
    Article
  17. Article
  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

5 authors at 1 institution in 1 country.

Narendra V SankpalSection of Endocrine and Oncologic Surgery, Washington University School of Medicine, St Louis, Missouri 63110, USA.
Michael W Willman
Timothy P Fleming
John D Mayfield
William E Gillanders
Washington University in St. Louis · US

Funding

Washington University Center for Cellular ImagingP30CA091842 · NCI · WASHINGTON UNIVERSITY · PI TIMOTHY J. EBERLEIN · 2001 to 2026
$128.0M
SURGICAL ONCOLOGY TRAINING GRANTT32CA009621 · NCI · WASHINGTON UNIVERSITY · PI TIMOTHY J. EBERLEIN, William E. Gillanders · 1988 to 2026
$12.9M
NCI NIH HHS P30 CA091842NCI NIH HHS T32 CA009621
6 · The paper itself

Abstract

p53 is a tumor suppressor gene with well-characterized roles in cell cycle regulation, apoptosis, and maintenance of genome stability. Recent evidence suggests that p53 may also contribute to the regulation of migration and invasion. Epithelial cell adhesion molecule (EpCAM) is a transmembrane glycoprotein that is overexpressed in the majority of human epithelial carcinomas, including breast and colorectal carcinomas. We show by chromatin immunoprecipitation assays that p53 interacts with a candidate p53 binding site within the EpCAM gene. p53-mediated transcriptional repression of EpCAM was confirmed in gain-of-function and loss-of-function experimental systems. Induction of wild-type p53 was associated with a significant dose-dependent decrease in EpCAM expression; conversely, specific ablation of p53 was associated with a significant increase in EpCAM expression. At the functional level, specific ablation of p53 expression is associated with increased breast cancer invasion, and this effect is abrogated by concomitant specific ablation of EpCAM expression. Taken together, these biochemical and functional data are the first demonstration that (a) wild-type p53 protein binds to a response element within the EpCAM gene and negatively regulates EpCAM expression, and (b) transcriptional repression of EpCAM contributes to p53 control of breast cancer invasion.

Indexed as

Antigens, NeoplasmBase SequenceBinding SitesBreast NeoplasmsCell Adhesion MoleculesCell Line, TumorChromatin ImmunoprecipitationEpithelial Cell Adhesion MoleculeGene Expression Regulation, NeoplasticHCT116 CellsHumansMolecular Sequence DataNeoplasm InvasivenessProtein ConformationTranscription, GeneticTumor Suppressor Protein p53Antigens, NeoplasmCell Adhesion MoleculesEPCAM protein, humanEpithelial Cell Adhesion MoleculeTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID19141643
PMCPMC3907266
OpenAlexW2137143355

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.