Evidence map›Paper›PMID 36215227›Full record

ArticleNeuro-oncology2023

Homeobox A3 and KDM6A cooperate in transcriptional control of aerobic glycolysis and glioblastoma progression.

Rui Yang, Guanghui Zhang, Zhen Dong, Shanshan Wang, Yanping Li, Fuming Lian, Xiaoran Liu, Haibin Li, Xiaonan Wei, Hongjuan Cui

Open access · greenAbstract read
In one paragraph

Article in Neuro-oncology, 2023. 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
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

24 citing papers in PubMed, 37 citations in OpenAlex.

  1. Review
  2. Sex differences in brain glucose metabolism and Alzheimer's disease risk and progression.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
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  18. LncRNA-Mediated TPI1 and PKM2 Promote Self-Renewal and Chemoresistance in GBM.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Article
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  20. Article
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 2 institutions in 1 country.

Rui YangInstitute of Precision Medicine, Jining Medical University, Jining 272067, China.ORCID 0000-0002-0525-1728
Guanghui ZhangCancer Center, Medical Research Institute, Southwest University, Chongqing 400716, China.
Zhen DongCancer Center, Medical Research Institute, Southwest University, Chongqing 400716, China.
Shanshan WangInstitute of Precision Medicine, Jining Medical University, Jining 272067, China.
Yanping LiInstitute of Precision Medicine, Jining Medical University, Jining 272067, China.
Fuming LianInstitute of Precision Medicine, Jining Medical University, Jining 272067, China.
Xiaoran LiuInstitute of Precision Medicine, Jining Medical University, Jining 272067, China.
Haibin LiInstitute of Precision Medicine, Jining Medical University, Jining 272067, China.
Xiaonan WeiInstitute of Precision Medicine, Jining Medical University, Jining 272067, China.
Hongjuan CuiCancer Center, Medical Research Institute, Southwest University, Chongqing 400716, China.
Jining Medical University · CNSouthwest University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAlterations in transcriptional regulators of glycolytic metabolism have been implicated in brain tumor growth, but the underlying molecular mechanisms remain poorly understood.

methodsKnockdown and overexpression cells were used to explore the functional roles of HOXA3 in cell proliferation, tumor formation, and aerobic glycolysis. Chromatin immunoprecipitation, luciferase assays, and western blotting were performed to verify the regulation of HK2 and PKM2 by HOXA3. PLA, Immunoprecipitation, and GST-pull-down assays were used to examine the interaction of HOXA3 and KDM6A.

resultsWe report that transcription factor homeobox A3 (HOXA3), which is aberrantly highly expressed in glioblastoma (GBM) patients and predicts poor prognosis, transcriptionally activates aerobic glycolysis, leading to a significant acceleration in cell proliferation and tumor growth. Mechanically, we identified KDM6A, a lysine-specific demethylase, as an important cooperator of HOXA3 in regulating aerobic glycolysis. HOXA3 activates KDM6A transcription and recruits KDM6A to genomic binding sites of glycolytic genes, targeting glycolytic genes for transcriptional activation by removing the suppressive histone modification H3K27 trimethylation. Further evidence demonstrates that HOXA3 requires KDM6A for transcriptional activation of aerobic glycolysis and brain tumor growth.

conclusionsOur findings provide a novel molecular mechanism linking HOXA3-mediated transactivation and KDM6A-coupled H3K27 demethylation in regulating glucose metabolism and GBM progression.

Indexed as

Brain NeoplasmsGlioblastomaCell Line, TumorGene Expression Regulation, NeoplasticGenes, HomeoboxGlycolysisHistone DemethylasesHumansTranscription FactorsHistone DemethylasesTranscription Factorsaerobic glycolysisGBMHOXA3KDM6Atranscriptional activation

Identifiers

PMID36215227
PMCPMC10076951
OpenAlexW4304114153

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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.