Evidence map›Paper›PMID 38093312›Full record

ArticleClinical epigenetics2023

Histone demethylase KDM4B accelerates the progression of glioblastoma via the epigenetic regulation of MYC stability.

Zhongze Wang, Huarui Cai, Zekun Li, Wei Sun, Erhu Zhao, Hongjuan Cui

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Clinical epigenetics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

10 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Targeting MYC-Driven Cancers: From Oncogenic Addiction to Therapeutic Vulnerability.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2026
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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

6 authors at 1 institution in 1 country.

Zhongze Wang *State Key Laboratory of Resource Insects, Medical Research Institute, Southwest University, No.2 Tiansheng Road, Beibei district, Chongqing, 400715, China.
Huarui Cai *State Key Laboratory of Resource Insects, Medical Research Institute, Southwest University, No.2 Tiansheng Road, Beibei district, Chongqing, 400715, China.
Zekun LiState Key Laboratory of Resource Insects, Medical Research Institute, Southwest University, No.2 Tiansheng Road, Beibei district, Chongqing, 400715, China.
Wei SunState Key Laboratory of Resource Insects, Medical Research Institute, Southwest University, No.2 Tiansheng Road, Beibei district, Chongqing, 400715, China.
Erhu ZhaoState Key Laboratory of Resource Insects, Medical Research Institute, Southwest University, No.2 Tiansheng Road, Beibei district, Chongqing, 400715, China. erhuzhao@126.com.
Hongjuan CuiState Key Laboratory of Resource Insects, Medical Research Institute, Southwest University, No.2 Tiansheng Road, Beibei district, Chongqing, 400715, China. hcui@swu.edu.cn.
Southwest University · CN

Funding

the Graduate Scientific Research Innovation Project of Chongqing CYS22255the Natural Science Foundation of Chongqing CSTB2022NSCQ-MSX0631, cstc2022ycjh-bgzxm0113
6 · The paper itself

Abstract

backgroundGlioblastoma (GBM) is the most malignant and invasive human brain tumor. Histone demethylase 4B (KDM4B) is abnormally expressed in GBM, but the molecular mechanisms by which KDM4B affects the malignant tumor progression are not well defined.

methodsGBM cell lines and xenograft tumor samples were subjected to quantitative PCR (qPCR), Western blot, immunohistochemical staining (IHC), as well as ubiquitination, immunoprecipitation (IP), and chromatin immunoprecipitation (ChIP) assays to investigate the role of KDM4B in the progression of GBM.

resultsHere, we report that KDM4B is an epigenetic activator of GBM progression. Abnormal expression of KDM4B is correlated with a poor prognosis in GBM patients. In GBM cell lines, KDM4B silencing significantly inhibited cell survival, proliferation, migration, and invasion, indicating that KDM4B is essential for the anchorage-independent growth and tumorigenic activity of GBM cells. Mechanistically, KDM4B silencing led to downregulation of the oncoprotein MYC and suppressed the expression of cell cycle proteins and epithelial-to-mesenchymal transition (EMT)-related proteins. Furthermore, we found that KDM4B regulates MYC stability through the E3 ligase complex SCF

conclusionsOur study has uncovered a KDM4B-dependent epigenetic mechanism in the control of tumor progression, providing a rationale for utilizing KDM4B as a promising therapeutic target for the treatment of MYC-amplified GBM.

Indexed as

GlioblastomaMicroRNAsCell Line, TumorCell ProliferationChromatin ImmunoprecipitationDNA MethylationEpigenesis, GeneticHistone DemethylasesHumansJumonji Domain-Containing Histone DemethylasesProto-Oncogene Proteins c-mycHistone DemethylasesJumonji Domain-Containing Histone DemethylasesKDM4B protein, humanMicroRNAsMYC protein, humanProto-Oncogene Proteins c-mycEpigenetic regulationKDM4BmiR-181d-5pMYCTumor progression

Identifiers

PMID38093312
PMCPMC10720090
OpenAlexW4389674472

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LicenceCC BY
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Registered trials

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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.