Evidence map›Paper›PMID 26731476›Full record

ArticleThe Journal of clinical investigation2016

Histone demethylase JMJD2A drives prostate tumorigenesis through transcription factor ETV1.

Tae-Dong Kim, Fang Jin, Sook Shin, Sangphil Oh, Stan A Lightfoot, Joseph P Grande, Aaron J Johnson, Jan M van Deursen, Jonathan D Wren, Ralf Janknecht

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed, 1 pooled it
6.6field-weighted citation impact, top 3% 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

69 citing papers in PubMed, 1 synthesis or guideline pooled it, 107 citations in OpenAlex.

  1. Pooled it
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  17. Article
  18. Epigenetic (De)regulation in Prostate Cancer.Cancer treatment and research · 2023
    Article
  19. Review
  20. Article

9 more citing papers are in PubMed but not listed here.

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 3 institutions in 1 country.

Tae-Dong Kim
Fang Jin
Sook Shin
Sangphil Oh
Stan A Lightfoot
Joseph P Grande
Aaron J Johnson
Jan M van Deursen
Jonathan D Wren
Ralf Janknecht
University of Oklahoma Health Sciences Center · USMayo Clinic · USOklahoma State University Oklahoma City · US

Funding

Tracking and Evaluation CoreU54GM104938 · NIGMS · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI Janis E Campbell · 2013 to 2026
$68.2M
TUMOR RESISTANCE MECHANISMS TO ANTI-VEGF THERAPY IN PROSTATE CANCER (Sukyung Woo)P20GM103639 · NIGMS · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI HANNAFON, BETHANY · 2012 to 2022
$21.3M
ETV1 and JMJD2 Demethylases in Prostate CancerR01CA154745 · NCI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI JANKNECHT, RALF · 2011 to 2015
$1.5M
NCI NIH HHS R01 CA154745NIGMS NIH HHS P20 GM103639NIGMS NIH HHS U54 GM104938
6 · The paper itself

Abstract

Histone demethylase upregulation has been observed in human cancers, yet it is unknown whether this is a bystander event or a driver of tumorigenesis. We found that overexpression of lysine-specific demethylase 4A (KDM4A, also known as JMJD2A) was positively correlated with Gleason score and metastasis in human prostate tumors. Overexpression of JMJD2A resulted in the development of prostatic intraepithelial neoplasia in mice, demonstrating that JMJD2A can initiate prostate cancer development. Moreover, combined overexpression of JMJD2A and the ETS transcription factor ETV1, a JMJD2A-binding protein, resulted in prostate carcinoma formation in mice haplodeficient for the phosphatase and tensin homolog (Pten) tumor-suppressor gene. Additionally, JMJD2A cooperated with ETV1 to increase expression of yes associated protein 1 (YAP1), a Hippo pathway component that itself was associated with prostate tumor aggressiveness. ETV1 facilitated the recruitment of JMJD2A to the YAP1 promoter, leading to changes in histone lysine methylation in a human prostate cancer cell line. Further, YAP1 expression largely rescued the growth inhibitory effects of JMJD2A depletion in prostate cancer cells, indicating that YAP1 is a downstream effector of JMJD2A. Taken together, these data reveal a JMJD2A/ETV1/YAP1 axis that promotes prostate cancer initiation and that may be a suitable target for therapeutic inhibition.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsCell Cycle ProteinsCell Line, TumorCell Transformation, NeoplasticDNA-Binding ProteinsFemaleHistone DemethylasesHumansJumonji Domain-Containing Histone DemethylasesMaleMiceMice, TransgenicNeoplasm ProteinsPhosphoproteinsProstatic NeoplasmsAdaptor Proteins, Signal TransducingCell Cycle ProteinsDNA-Binding ProteinsETV1 protein, humanEtv1 protein, mouseHistone DemethylasesJMJD2A protein, mouseJumonji Domain-Containing Histone DemethylasesKDM4A protein, humanNeoplasm ProteinsPhosphoproteinsTranscription FactorsYAP1 protein, humanYap1 protein, mouseYAP-Signaling Proteins

Identifiers

PMID26731476
PMCPMC4731184
OpenAlexW2228585033

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.