Evidence map›Paper›PMID 40229896›Full record

ArticleEuropean journal of medical research2025

The KDM5A/HOXA5 axis regulates osteosarcoma progression via activating the Wnt/β-catenin pathway.

Yi Luo, Youzhi He, Yuxia Xu, Yongfu Wang, Li Yang

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in European journal of medical research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
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

4 citing papers in PubMed.

  1. Review
  2. Review
  3. Review
  4. NFATC3 enhances osteosarcoma progression by increasing PD-L1 and CXCL2 levels.Medical oncology (Northwood, London, England) · 2025
    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

5 authors.

Yi LuoDepartment of Spine Surgery, Hengyang Medical School, The Affiliated Changsha Central Hospital, University of South China, The No.161 of the Shaoshan South Road, Changsha City, Hunan Province, China. luoyi8166@126.com.
Youzhi HeDepartment of Spine Surgery, Hengyang Medical School, The Affiliated Changsha Central Hospital, University of South China, The No.161 of the Shaoshan South Road, Changsha City, Hunan Province, China.
Yuxia XuDepartment of Spine Surgery, Hengyang Medical School, The Affiliated Changsha Central Hospital, University of South China, The No.161 of the Shaoshan South Road, Changsha City, Hunan Province, China.
Yongfu WangDepartment of Spine Surgery, Hengyang Medical School, The Affiliated Changsha Central Hospital, University of South China, The No.161 of the Shaoshan South Road, Changsha City, Hunan Province, China.
Li YangDepartment of Spine Surgery, Hengyang Medical School, The Affiliated Changsha Central Hospital, University of South China, The No.161 of the Shaoshan South Road, Changsha City, Hunan Province, China.

Funding

Changsha Natural Science Foundation general project kq2202050
6 · The paper itself

Abstract

As an oncogenic driver, lysine-specific demethylase 5A (KDM5A) participates in regulating numerous tumor progression-related processes. Moreover, KDM5A functions as a histone demethylase, modulating the expression levels of its target genes by adjusting methylation levels. However, the underlying molecular mechanism of KDM5A in osteosarcoma remains elusive. To elucidate this mechanism, specifically how the KDM5A /Homeobox A5 (HOXA5) axis regulates osteosarcoma progression, we measured the expression levels of KDM5A and HOXA5 genes using reverse transcription-quantitative real-time PCR. The correlation between HOXA5 and KDM5A was analyzed via Pearson correlation analysis and further validated through chromatin immunoprecipitation-quantitative real-time PCR. Immunohistochemistry was conducted to determine the number of KDM5A-or HOXA5-positive cells present in osteosarcoma tissues. Additionally, Western blot analysis was utilized to quantify the protein levels of KDM5A, HOXA5, di- and tri-methylation of lysine 4 on histone H3, and β-catenin. Colony formation assays, wound healing assays and flow cytometry were used to detect cell proliferation, migration and apoptosis. The factors associated with the five-year survival rate of patients were analyzed. Our results illustrated that KDM5A was up-regulated in osteosarcoma and associated with a poor prognosis; KDM5A knockdown inhibited osteosarcoma cell proliferation and migration and promotes apoptosis. Subsequently, KDM5A knockdown induced HOXA5 expression by promoting di- and tri-methylation of lysine 4 on histone H3 demethylation, and HOXA5 overexpression inhibited osteosarcoma cell proliferation and migration, and promoted apoptosis by inhibiting the Wnt/β-catenin pathway. We finally proved that HOXA5 silence weakened the inhibitory effect of sh- KDM5A on osteosarcoma proliferation and migration and promoted apoptosis via activating Wnt/β-catenin pathway in vivo and in vitro. Our study demonstrated that the KDM5A /HOXA5 axis regulates osteosarcoma progression by activating the Wnt/β-catenin pathway.

Indexed as

Bone NeoplasmsHomeodomain ProteinsOsteosarcomaRetinoblastoma-Binding Protein 2Wnt Signaling PathwayApoptosisbeta CateninCell Line, TumorCell MovementCell ProliferationDisease ProgressionFemaleGene Expression Regulation, NeoplasticHumansMalePrognosisbeta CateninHomeodomain ProteinsHOXA5 protein, humanKDM5A protein, humanRetinoblastoma-Binding Protein 2Di- and tri-methylation of lysine 4 on histone H3Homeobox A5Lysine-specific demethylase 5AMethylation modificationOsteosarcoma

Identifiers

PMID40229896
PMCPMC11998425

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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.