Evidence map›Paper›PMID 40113969›Full record

ArticleNPJ precision oncology2025

Multi-omics analysis identifies glioblastoma dependency on H3K9me3 methyltransferase activity.

Qiqi Xie, Yuanning Du, Sugata Ghosh, Saranya Rajendran, Aaron A Cohen-Gadol, José-Manuel Baizabal, Kenneth P Nephew, Leng Han, Jia Shen

Abstract read
In one paragraph

Article in NPJ precision oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing 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

7 citing papers in PubMed.

  1. Article
  2. 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

9 authors.

Qiqi XieMedical Sciences Program, Indiana University School of Medicine, Bloomington, IN, 47405, USA.ORCID http://orcid.org/0000-0003-4099-5287
Yuanning DuMedical Sciences Program, Indiana University School of Medicine, Bloomington, IN, 47405, USA.
Sugata GhoshMedical Sciences Program, Indiana University School of Medicine, Bloomington, IN, 47405, USA.
Saranya RajendranMedical Sciences Program, Indiana University School of Medicine, Bloomington, IN, 47405, USA.
Aaron A Cohen-GadolDepartment of Neurological Surgery, Indiana University School of Medicine, Indianapolis, IN, 46202, USA.
José-Manuel BaizabalDepartment of Biology, Indiana University, Bloomington, IN, 47405, USA.
Kenneth P NephewMedical Sciences Program, Indiana University School of Medicine, Bloomington, IN, 47405, USA.ORCID http://orcid.org/0000-0003-2192-1346
Leng HanBrown Center for Immunotherapy, Indiana University School of Medicine, Indianapolis, IN, 46202, USA. lenghan@iu.edu.ORCID http://orcid.org/0000-0002-7380-2640
Jia ShenMedical Sciences Program, Indiana University School of Medicine, Bloomington, IN, 47405, USA. shen17@iu.edu.

Funding

Systematic Characterization of Small Nucleolar RNAs in CancerR01CA262623 · NCI · TEXAS A&M UNIVERSITY HEALTH SCIENCE CTR · PI HAN, LENG · 2021 to 2025
$2.0M
MolQTL: A comprehensive resource for molecular quantitative trait loci inhuman cancer.R01HG011633 · NHGRI · TEXAS A&M UNIVERSITY HEALTH SCIENCE CTR · PI HAN, LENG · 2021 to 2025
$1.9M
NCI NIH HHS R01 CA262623NHGRI NIH HHS R01 HG011633U.S. Department of Health & Human Services | National Institutes of Health (NIH) R01CA262623U.S. Department of Health & Human Services | National Institutes of Health (NIH) R01HG011633
6 · The paper itself

Abstract

Histone H3 lysine 9 dimethylation and trimethylation (H3K9me2/3) are prevalent in human genomes, especially in heterochromatin and specific euchromatic genes. Methylation of H3K9 is modulated by enzymes such as SUV39H1, SUV39H2, SETDB1, SETDB2, and EHMT1/2, which influence cancer progression. This study reveals differential expression of these six H3K9 methyltransferases in tumors, with SUV39H1, SUV39H2, and SETDB1 showing significant links to cancer phenotypes. We developed the "H3K9me3 MtSig" (H3K9me3 methyltransferases signature) based on these findings. H3K9me3 MtSig is unique to various tumors, with prognostic significance and associations with key signaling pathways, especially in glioblastoma (GBM). Elevated H3K9me3 MtSig was observed in GBM samples, correlating with the G2/M cell cycle and reduced immune responses. H3K9me3-mediated repetitive sequence silencing by H3K9me3 MtSig contributed to these phenotypes, and inhibiting H3K9me3 MtSig in patient-derived GBM cells suppressed proliferation and increased immune responses. H3K9me3 MtSig serves as an independent prognostic factor and potential therapeutic target.

Identifiers

PMID40113969
PMCPMC11926169

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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.