Evidence map›Paper›PMID 21446014›Full record

ArticleThe Prostate2011

Mechanisms and functional consequences of PDEF protein expression loss during prostate cancer progression.

David P Turner, Victoria J Findlay, Omar Moussa, Victor I Semenchenko, Patricia M Watson, Amanda C LaRue, Mohamed M Desouki, Mostafa Fraig, Dennis K Watson

Abstract read
In one paragraph

Article in The Prostate, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

38 citing papers in PubMed, 59 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Double Agent:Cancer management and research · 2020
    Review
  9. Article
  10. Article
  11. International journal of molecular sciences · 2019
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Signatures of prostate-derived Ets factor (PDEF) in cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    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

9 authors at 2 institutions in 1 country.

David P TurnerDepartment of Pathology and Laboratory Medicine, Medical University of South Carolina, Charleston, SC, USA.
Victoria J Findlay
Omar Moussa
Victor I Semenchenko
Patricia M Watson
Amanda C LaRue
Mohamed M Desouki
Mostafa Fraig
Dennis K Watson
MUSC Hollings Cancer Center · USMedical University of South Carolina · US

Funding

Translational Science Laboratory Shared ResourceP30CA138313 · NCI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI RAYMOND N. DUBOIS · 2009 to 2026
$42.7M
THE ROLE OF FLI1 IN CELLULAR DIFFERENTIATION AND DEVELOPMENTP01CA078582 · NCI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI TROJANOWSKA, MARIA · 1998 to 2009
$9.1M
Hematopoietic Stem Cell-Derived Carcinoma Associated Fibroblasts in TumorR01CA148772 · NCI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI LARUE, AMANDA C. · 2011 to 2015
$1.3M
NCI NIH HHS P01 CA078582NCI NIH HHS P01CA78582NCI NIH HHS P30 CA 138313NCI NIH HHS P30 CA138313NCI NIH HHS R01 CA148772
6 · The paper itself

Abstract

backgroundEts is a large family of transcriptional regulators with functions in most biological processes. While the Ets family gene, prostate-derived epithelial factor (PDEF), is expressed in epithelial tissues, PDEF protein expression has been found to be reduced or lost during cancer progression. The goal of this study was to examine the mechanism for and biologic impact of altered PDEF expression in prostate cancer.

methodsPDEF protein expression of prostate specimens was examined by immunohistochemistry. RNA and protein expression in cell lines were measured by q-PCR and Western blot, respectively. Cellular growth was determined by quantifying viable and apoptotic cells over time. Cell cycle was measured by flow cytometry. Migration and invasion were determined by transwell assays. PDEF promoter occupancy was determined by chromatin immunoprecipitation (ChIP).

resultsWhile normal prostate epithelium expresses PDEF mRNA and protein, tumors show no or decreased PDEF protein expression. Re-expression of PDEF in prostate cancer cells inhibits cell growth. PDEF expression is inversely correlated with survivin, urokinase plasminogen activator (uPA) and slug expression and ChIP studies identify survivin and uPA as direct transcriptional targets of PDEF. This study also shows that PDEF expression is regulated via a functional microRNA-204 (miR-204) binding site within the 3'UTR. Furthermore, we demonstrate the biologic significance of miR-204 expression and that miR-204 is over-expressed in human prostate cancer specimens.

conclusionsCollectively, the reported studies demonstrate that PDEF is a negative regulator of tumor progression and that the miR-204-PDEF regulatory axis contributes to PDEF protein loss and resultant cancer progression.

Indexed as

Cell CycleCell Line, TumorCell MovementCell NucleusCell ProliferationDisease ProgressionGene Expression Regulation, EnzymologicHumansMaleMicroRNAsNeoplasm InvasivenessProstatic NeoplasmsProto-Oncogene Proteins c-etsMicroRNAsMIRN204 microRNA, humanProto-Oncogene Proteins c-etsSPDEF protein, human

Identifiers

PMID21446014
PMCPMC3128180
OpenAlexW2027519787

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.