Evidence map›Paper›PMID 24362521›Full record

ArticleOncogene2015

The histone demethylase KDM3A is a microRNA-22-regulated tumor promoter in Ewing Sarcoma.

J K Parrish, M Sechler, R A Winn, P Jedlicka

Abstract read
In one paragraph

Article in Oncogene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

50 citing papers in PubMed, 83 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Unlocking epigenetics for precision treatment of Ewing's sarcoma.Chinese journal of cancer research = Chung-kuo yen cheng yen chiu · 2024
    Article
  5. Fli1 and Tissue Fibrosis in Various Diseases.International journal of molecular sciences · 2023
    Review
  6. Article
  7. Review
  8. Review
  9. Review
  10. Article
  11. Review
  12. Review
  13. Hairless regulates heterochromatin maintenance and muscle stem cell function as a histone demethylase antagonist.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
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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

4 authors at 3 institutions in 1 country.

J K ParrishDepartment of Pathology, University of Colorado Denver, Anschutz Medical Campus, Aurora, CO, USA.
M SechlerCancer Biology Graduate Program, University of Colorado Denver, Anschutz Medical Campus, Aurora, CO, USA.
R A WinnDepartment of Medicine, University of Illinois, Chicago, IL, USA.
P Jedlicka1] Department of Pathology, University of Colorado Denver, Anschutz Medical Campus, Aurora, CO, USA [2] Cancer Biology Graduate Program, University of Colorado Denver, Anschutz Medical Campus, Aurora, CO, USA.
University of Colorado Cancer Center · USUniversity of Colorado Anschutz Medical Campus · USUniversity of Illinois Chicago · US

Funding

University of Colorado Cancer Center Support Grant - Lung Cancer Patient-Derived Xenografts with Autologous Human Immune SystemsP30CA046934 · NCI · UNIVERSITY OF COLORADO DENVER · PI James V Degregori · 1988 to 2026
$117.0M
Role of the noncanonical WNT pathway in non-small cell lung cancerR01CA138528 · NCI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI WINN, ROBERT A. · 2010 to 2014
$1.4M
NCI NIH HHS P30 CA046934NCI NIH HHS R01 CA138528NCI NIH HHS R01CA138528-2522717
6 · The paper itself

Abstract

Ewing Sarcoma is a biologically aggressive bone and soft tissue malignancy affecting children and young adults. Ewing Sarcoma pathogenesis is driven by EWS/Ets fusion oncoproteins, of which EWS/Fli1 is the most common. We have previously shown that microRNAs (miRs) regulated by EWS/Fli1 contribute to the pro-oncogenic program in Ewing Sarcoma. Here we show that miR-22, an EWS/Fli1-repressed miR, is inhibitory to Ewing Sarcoma clonogenic and anchorage-independent cell growth, even at modest overexpression levels. Our studies further identify the H3K9me1/2 histone demethylase KDM3A (JMJD1A/JHDM2A) as a new miR-22-regulated gene. We show that KDM3A is overexpressed in Ewing Sarcoma, and that its depletion inhibits clonogenic and anchorage-independent growth in multiple patient-derived cell lines, and tumorigenesis in a xenograft model. KDM3A depletion further results in augmentation of the levels of the repressive H3K9me2 histone mark, and downregulation of pro-oncogenic factors in Ewing Sarcoma. Together, our studies identify the histone demethylase KDM3A as a new, miR-regulated, tumor promoter in Ewing Sarcoma.

Indexed as

AnimalsBone NeoplasmsCell Line, TumorCell Transformation, NeoplasticDown-RegulationEpigenomicsHeterograftsHumansJumonji Domain-Containing Histone DemethylasesMiceMice, NudeMicroRNAsSarcoma, EwingJumonji Domain-Containing Histone DemethylasesKDM3A protein, humanMicroRNAsMIRN22 microRNA, human

Identifiers

PMID24362521
PMCPMC4477825
OpenAlexW2084826637

What OpenQuestion holds

Textmetadata
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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.