Evidence map›Paper›PMID 35440714›Full record

ArticleOncogene2022

H3K4 demethylase KDM5B regulates cancer cell identity and epigenetic plasticity.

Runsheng He, Besa Xhabija, Lijin K Gopi, Jiji T Kurup, Zhishan Xu, Zhe Liu, Benjamin L Kidder

Open access · greenAbstract read
In one paragraph

Article in Oncogene, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.9field-weighted citation impact, top 8% 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

17 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
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  8. Review
  9. KDM5D histone demethylase mediates p38α inactivation via its enzymatic activity to inhibit cancer progression.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  10. Article
  11. CanPharmaceuticals (Basel, Switzerland) · 2024
    Review
  12. Article
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  15. Review
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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

7 authors at 2 institutions in 2 countries.

Runsheng HeDepartment of Oncology, Wayne State University School of Medicine, Detroit, MI, USA.
Besa XhabijaDepartment of Oncology, Wayne State University School of Medicine, Detroit, MI, USA.
Lijin K GopiDepartment of Oncology, Wayne State University School of Medicine, Detroit, MI, USA.
Jiji T KurupDepartment of Oncology, Wayne State University School of Medicine, Detroit, MI, USA.
Zhishan XuDepartment of Oncology, Wayne State University School of Medicine, Detroit, MI, USA.
Zhe LiuDepartment of Chemistry and Chemical Engineering, Qufu Normal University, Qufu, 273165, Shandong, PR China.
Benjamin L KidderDepartment of Oncology, Wayne State University School of Medicine, Detroit, MI, USA. benjamin.kidder@wayne.edu.ORCID http://orcid.org/0000-0002-2039-7143
Wayne State University · USQufu Normal University · CN

Funding

Tumor Biology and Microenvironment (Program 1)P30CA022453 · NCI · WAYNE STATE UNIVERSITY · PI Julie Lynn Boerner · 1985 to 2026
$68.4M
NCI NIH HHS P30 CA022453
6 · The paper itself

Abstract

The H3K4 demethylase KDM5B is overexpressed in multiple cancer types, and elevated expression levels of KDM5B is associated with decreased survival. However, the underlying mechanistic contribution of dysregulated expression of KDM5B and H3K4 demethylation in cancer is poorly understood. Our results show that loss of KDM5B in multiple types of cancer cells leads to increased proliferation and elevated expression of cancer stem cell markers. In addition, we observed enhanced tumor formation following KDM5B depletion in a subset of representative cancer cell lines. Our findings also support a role for KDM5B in regulating epigenetic plasticity, where loss of KDM5B in cancer cells with elevated KDM5B expression leads to alterations in activity of chromatin states, which facilitate activation or repression of alternative transcriptional programs. In addition, we define KDM5B-centric epigenetic and transcriptional patterns that support cancer cell plasticity, where KDM5B depleted cancer cells exhibit altered epigenetic and transcriptional profiles resembling a more primitive cellular state. This study also provides a resource for evaluating associations between alterations in epigenetic patterning upon depletion of KDM5B and gene expression in a diverse set of cancer cells.

Indexed as

Jumonji Domain-Containing Histone DemethylasesNeoplasmsCell Line, TumorEpigenesis, GeneticEpigenomicsHumansNuclear ProteinsRepressor ProteinsJumonji Domain-Containing Histone DemethylasesKDM5B protein, humanNuclear ProteinsRepressor Proteins

Identifiers

PMID35440714
PMCPMC9426628
OpenAlexW4224226948

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.