Evidence map›Paper›PMID 41096621›Full record

ArticleInternational journal of molecular sciences2025

The HMGB1-RAGE Axis Drives the Proneural-to-Mesenchymal Transition and Aggressiveness in Glioblastoma.

Hao-Chien Yang, Yu-Kai Su, Vijesh Kumar Yadav, Iat-Hang Fong, Heng-Wei Liu, Chien-Min Lin

Abstract read
In one paragraph

Article in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

6 authors.

Hao-Chien YangDivision of Neurosurgery, Department of Surgery, Taipei Medical University-Shuang Ho Hospital, New Taipei City 23561, Taiwan.
Yu-Kai SuDivision of Neurosurgery, Department of Surgery, Taipei Medical University-Shuang Ho Hospital, New Taipei City 23561, Taiwan.
Vijesh Kumar YadavDepartment of Medical Research & Education, Taipei Medical University-Shuang Ho Hospital, New Taipei City 23561, Taiwan.ORCID 0000-0002-2679-1205
Iat-Hang FongDivision of Neurosurgery, Department of Surgery, Taipei Medical University-Shuang Ho Hospital, New Taipei City 23561, Taiwan.ORCID 0000-0002-8235-0877
Heng-Wei LiuDivision of Neurosurgery, Department of Surgery, Taipei Medical University-Shuang Ho Hospital, New Taipei City 23561, Taiwan.
Chien-Min LinDivision of Neurosurgery, Department of Surgery, Taipei Medical University-Shuang Ho Hospital, New Taipei City 23561, Taiwan.ORCID 0000-0001-5404-0145

Funding

Taipei Medical University-Shuang Ho Hospital NSTC111-2314-B038-133-MY3Taipei Medical University-Shuang Ho Hospital NSTC 113-2314-B-038-118-MY3
6 · The paper itself

Abstract

Glioblastoma (GBM) remains the most lethal primary brain tumor, owing to profound intratumoral heterogeneity and the limited efficacy of standard treatments. The mesenchymal (MES) molecular subtype is particularly aggressive, exhibiting heightened invasiveness, therapy resistance, and dismal patient survival compared with the proneural (PN) subtype. Emerging evidence implicates the High Mobility Group Box 1 (HMGB1) protein and its cognate receptor, the Receptor for Advanced Glycation End Products (RAGE), as drivers of malignant progression, yet their contribution to the PN-to-MES transition is incompletely defined. We integrated transcriptomic analyses of TCGA-GBM and TCGA-LGG cohorts with immunohistochemistry on in-house patient specimens. Functional studies in patient-derived and established GBM cell lines included migration and invasion assays, tumorsphere formation assays, shRNA knockdowns, and Seahorse XF metabolic profiling to interrogate the HMGB1-RAGE axis. HMGB1 and RAGE expression was markedly elevated in MES GBM tissues and cell lines. Importantly, higher HMGB1 expression correlated with shortened overall survival (

Indexed as

Brain NeoplasmsEpithelial-Mesenchymal TransitionGlioblastomaHMGB1 ProteinReceptor for Advanced Glycation End ProductsCell Line, TumorCell MovementGene Expression Regulation, NeoplasticHumansNeoplasm InvasivenessSignal TransductionHMGB1 ProteinHMGB1 protein, humanReceptor for Advanced Glycation End ProductsglioblastomaHMGB1-RAGE signalingmetabolic reprogrammingproneural-to-mesenchymal transitiontherapy resistancetumor stemness

Identifiers

PMID41096621
PMCPMC12524595

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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.