Evidence map›Paper›PMID 21212260›Full record

ArticleThe Journal of biological chemistry2011

Cyclin D1 is a selective modifier of androgen-dependent signaling and androgen receptor function.

Clay E S Comstock, Michael A Augello, Matthew J Schiewer, Jason Karch, Craig J Burd, Adam Ertel, Erik S Knudsen, Walter J Jessen, Bruce J Aronow, Karen E Knudsen

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
3.5field-weighted citation impact, top 6% 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

24 citing papers in PubMed, 42 citations in OpenAlex.

  1. A Randomized Phase II Study of Androgen Deprivation Therapy with or without Palbociclib in RB-positive Metastatic Hormone-Sensitive Prostate Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2021
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  17. Cyclin D2 is a GATA4 cofactor in cardiogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2014
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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

10 authors at 5 institutions in 1 country.

Clay E S ComstockFrom the Kimmel Cancer Center,; Department of Cancer Biology.
Michael A AugelloFrom the Kimmel Cancer Center,; Department of Cancer Biology.
Matthew J SchiewerFrom the Kimmel Cancer Center,; Department of Cancer Biology.
Jason Karchthe Department of Cell and Cancer Biology, University of Cincinnati, Cincinnati, Ohio 45221.
Craig J BurdNIEHS, National Institutes of Health, Research Triangle Park, North Carolina 27709.
Adam ErtelFrom the Kimmel Cancer Center,; Department of Cancer Biology.
Erik S KnudsenFrom the Kimmel Cancer Center,; Department of Cancer Biology.
Walter J Jessenthe Covance Biomarker Center of Excellence, Greenfield, Indiana 46140, and.
Bruce J AronowCincinnati Children's Hospital Medical Center, Cincinnati, Ohio 45229.
Karen E KnudsenFrom the Kimmel Cancer Center,; Department of Cancer Biology,; Department of Urology, and; Department of Radiation Oncology, Thomas Jefferson University, Philadelphia, Pennsylvania 19107,. Electronic address: Karen.Knudsen@kimmelcancercenter.org.
Sidney Kimmel Cancer Center · USCincinnati Children's Hospital Medical Center · USCovance (United States) · USNational Institutes of Health · USUniversity of Cincinnati · US

Funding

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
NCI NIH HHS CA099996NCI NIH HHS R01 CA099996
6 · The paper itself

Abstract

D-type cyclins regulate cellular outcomes in part through cyclin-dependent, kinase-independent mechanisms that modify transcription factor action, and recent in vivo studies showed that cyclin D1 associates with a large number of transcriptional regulators in cells of the retina and breast. Given the frequency of cyclin D1 alterations in cancer, it is imperative to delineate the molecular mechanisms by which cyclin D1 controls key transcription factor networks in human disease. Prostate cancer was used as a paradigm because this tumor type is reliant at all stages of the disease on androgen receptor (AR) signaling, and cyclin D1 has been shown to negatively modulate AR-dependent expression of prostate-specific antigen (KLK3/PSA). Strategies were employed to control cyclin D1 expression under conditions of hormone depletion, and the effect of cyclin D1 on subsequent androgen-dependent gene expression was determined using unbiased gene expression profiling. Modulating cyclin D1 conferred widespread effects on androgen signaling and revealed cyclin D1 to be a selective effector of hormone action. A subset of androgen-induced target genes, known to be directly regulated by AR, was strongly suppressed by cyclin D1. Analyses of AR occupancy at target gene regulatory loci of clinical relevance demonstrated that cyclin D1 limits AR residence after hormone stimulation. Together, these findings reveal a new function for cyclin D1 in controlling hormone-dependent transcriptional outcomes and demonstrate a pervasive role for cyclin D1 in regulating transcription factor dynamics.

Indexed as

Gene Expression Regulation, NeoplasticSignal TransductionAndrogensCell Line, TumorCyclin D1Genetic LociHumansKallikreinsMaleProstate-Specific AntigenProstatic NeoplasmsReceptors, AndrogenAndrogensCCND1 protein, humanCyclin D1KallikreinsKLK3 protein, humanProstate-Specific AntigenReceptors, Androgen

Identifiers

PMID21212260
PMCPMC3048698
OpenAlexW2070093704

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.