Evidence map›Paper›PMID 19784072›Full record

ArticleOncogene2010

Downregulation of E-cadherin is an essential event in activating beta-catenin/Tcf-dependent transcription and expression of its target genes in Pdcd4 knockdown cells.

Q Wang, Z-X Sun, H Allgayer, H-S Yang

Abstract read
In one paragraph

Article in Oncogene, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed, 1 pooled it
2.4field-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

59 citing papers in PubMed, 1 synthesis or guideline pooled it, 88 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. The Impact of Pdcd4, a Translation Inhibitor, on Drug Resistance.Pharmaceuticals (Basel, Switzerland) · 2024
    Review
  8. Review
  9. Article
  10. Atg7 senses ATP levels and regulates AKTCommunications biology · 2023
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. The role of LncRNA MALAT-1 and MiRNA-9 in Psoriasis.Biochemistry and biophysics reports · 2021
    Article
  17. Article
  18. 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

4 authors at 4 institutions in 3 countries.

Q WangGraduate Center for Toxicology, College of Medicine, University of Kentucky, Lexington, KY 40536, USA.
Z-X Sun
H Allgayer
H-S Yang
Beijing University of Chinese Medicine · CNMarkey Cancer Center · USThe Graduate Center, CUNY · USUniversity Medical Centre Mannheim · DE

Funding

UNDERSTANDING THE MOLECULAR BASIS OF EPIGENETIC TRANSCRIPTIONAL SILENCINGP20RR020171 · NCRR · UNIVERSITY OF KENTUCKY · PI LOUIS HERSH, LOUIS HERSH LOUIS HERSH · 2004 to 2011
$16.5M
The role of Pdcd4 in colorectal tumor progressionR01CA129015 · NCI · UNIVERSITY OF KENTUCKY · PI YANG, HSIN-SHENG · 2009 to 2013
$1.5M
NCI NIH HHS R01 CA129015NCI NIH HHS R01CA129015NCRR NIH HHS P20 RR020171NCRR NIH HHS P20RR020171
6 · The paper itself

Abstract

We reported earlier that knockdown of tumor suppressor Pdcd4 (programed cell death 4) downregulates E-cadherin expression and activates beta-catenin/Tcf (T-cell factor)-dependent transcription in colon tumor cells. However, the underlying mechanism of these observations remains unknown. In this study, we showed that knockdown of Pdcd4 downregulates E-cadherin expression through elevated protein level of Snail. Over-expression of Pdcd4 upregulates E-cadherin expression and inhibits beta-catenin/Tcf-dependent transcription. We then showed that knockdown of E-cadherin activates beta-catenin/Tcf-dependent transcription. Conversely, over-expression of E-cadherin in Pdcd4 knockdown cells inhibits beta-catenin/Tcf-dependent transcription. In addition, Pdcd4 knockdown stimulates urokinase-type plasminogen activator receptor (u-PAR) and c-Myc expression, whereas u-PAR and c-Myc expression can be reversed by over-expressing E-cadherin in Pdcd4 knockdown cells. Using chromatin immunoprecipitation, we showed that beta-catenin/Tcf4 directly binds to the promoters of u-PAR and c-myc in Pdcd4 knockdown cells. Futhermore, knockdown of u-PAR or c-Myc inhibits invasion in Pdcd4 knockdown cells, suggesting that both u-PAR and c-Myc contribute to invasion induced by Pdcd4 knockdown. Taken together, our data showed that elevated Snail expression by Pdcd4 knockdown leads to downregulation of E-cadherin resulting in activating beta-catenin/Tcf-dependent transcription and stimulating the expression of c-Myc and u-PAR, thus providing molecular explanation of how Pdcd4 suppresses tumor invasion.

Indexed as

Apoptosis Regulatory Proteinsbeta CateninBlotting, WesternCadherinsCell Line, TumorChromatin ImmunoprecipitationDown-RegulationGene Expression Regulation, NeoplasticGene Knockdown TechniquesHT29 CellsHumansMutationProtein BindingProto-Oncogene Proteins c-mycReceptors, Urokinase Plasminogen ActivatorReverse Transcriptase Polymerase Chain ReactionApoptosis Regulatory Proteinsbeta CateninCadherinsMYC protein, humanPDCD4 protein, humanProto-Oncogene Proteins c-mycReceptors, Urokinase Plasminogen ActivatorRNA-Binding ProteinsSnail Family Transcription FactorsTCF Transcription FactorsTranscription Factors

Identifiers

PMID19784072
PMCPMC2920641
OpenAlexW2014235909

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.