Evidence map›Paper›PMID 18084330›Full record

ArticleOncogene2008

Cyclin D3 action in androgen receptor regulation and prostate cancer.

N A Olshavsky, E M Groh, C E S Comstock, L M Morey, Y Wang, M P Revelo, C Burd, J Meller, K E Knudsen

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

19 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
  2. Article
  3. International journal of molecular sciences · 2023
    Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. The AR dependent cell cycle: mechanisms and cancer relevance.Molecular and cellular endocrinology · 2012
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. 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

9 authors at 3 institutions in 1 country.

N A OlshavskyDepartment of Cell and Cancer Biology, Vontz Center for Molecular Studies, University of Cincinnati College of Medicine, Cincinnati, OH 45267-0521, USA.
E M Groh
C E S Comstock
L M Morey
Y Wang
M P Revelo
C Burd
J Meller
K E Knudsen
University of Cincinnati Medical Center · USNational Institute of Environmental Health Sciences · USUniversity of Utah · US

Funding

ENVIRONMETAL CARCINOGENESIS AND MUTAGENESIST32ES007250 · NIEHS · UNIVERSITY OF CINCINNATI · PI MILLER, WILLIAM E · 1988 to 2024
$11.9M
Training Program in Cancer TherapeuticsT32CA117846 · NCI · UNIVERSITY OF CINCINNATI · PI PRICE, CAROLYN M, TAKIAR, VINITA · 2006 to 2022
$6.5M
Cyclin D1: repercussions of AR control and alternative splicing in prostate canceR01CA099996 · NCI · UNIVERSITY OF CINCINNATI · PI KNUDSEN, KAREN E · 2003 to 2013
$2.6M
Role of BAF57 in AR control and prostate cancer growthR01CA116777 · NCI · UNIVERSITY OF CINCINNATI · PI KNUDSEN, KAREN E · 2006 to 2010
$1.3M
NCI NIH HHS CA099996NCI NIH HHS CA116777NCI NIH HHS T32 CA117846NCI NIH HHS T32-CA117846NIEHS NIH HHS T32-ES07250
6 · The paper itself

Abstract

Prostate cancer (PCa) cell proliferation is dependent on activation of the androgen receptor (AR), a ligand-dependent transcription factor. AR activation controls G1-S phase progression through fostering enhanced translation of the D-type cyclins, which promote cell cycle progression through activation of CDK4/6. However, the D-type cyclins harbor additional, CDK4/6 kinase-independent, functions through manipulation of transcription factors, including AR. It was previously established that cyclins D1 and D3 have the potential to modulate AR, and with regard to cyclin D1, disruption of this function occurs in human tumors. Therefore, it was essential to interrogate cyclin D3 function in this tumor type. Here, we show that cyclin D3 is found in association with AR in PCa cells, as mediated through a conserved motif. Cyclin D3 functions to attenuate AR activity through defined mechanisms that include modulation of ligand-dependent conformational changes and modulation of chromatin binding activity. Accumulated cyclin D3 slows cell proliferation in AR-dependent cells, thus suggesting that androgen-induced D-type cyclin production serves to temper the mitogenic response to androgen. Supporting this hypothesis, it is shown that cyclin D3 expression is reduced in primary PCas as a function of tumor grade, and inversely correlates with the proliferative index. In total, these data identify cyclin D3 as a critical modulator of the androgen response, whose deregulation may foster unchecked AR activity in PCa.

Indexed as

Gene Expression Regulation, NeoplasticAdenocarcinomaAndrogensAnimalsCell ProliferationChlorocebus aethiopsCOS CellsCyclin DCyclin D3Cyclin-Dependent Kinase 4CyclinsDisease ProgressionHumansMaleNeoplasms, Hormone-DependentProstate-Specific AntigenAndrogensCCND3 protein, humanCyclin DCyclin D3Cyclin-Dependent Kinase 4CyclinsProstate-Specific AntigenReceptors, AndrogenRepressor Proteins

Identifiers

PMID18084330
OpenAlexW2078635517

What OpenQuestion holds

Textmetadata
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.