Multi-omics analysis identifies glioblastoma dependency on H3K9me3 methyltransferase activity

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 progressio...

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Main Authors: Qiqi Xie, Yuanning Du, Sugata Ghosh, Saranya Rajendran, Aaron A. Cohen-Gadol, José-Manuel Baizabal, Kenneth P. Nephew, Leng Han, Jia Shen
Format: Article
Language:English
Published: Nature Portfolio 2025-03-01
Series:npj Precision Oncology
Online Access:https://doi.org/10.1038/s41698-025-00829-5
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author Qiqi Xie
Yuanning Du
Sugata Ghosh
Saranya Rajendran
Aaron A. Cohen-Gadol
José-Manuel Baizabal
Kenneth P. Nephew
Leng Han
Jia Shen
author_facet Qiqi Xie
Yuanning Du
Sugata Ghosh
Saranya Rajendran
Aaron A. Cohen-Gadol
José-Manuel Baizabal
Kenneth P. Nephew
Leng Han
Jia Shen
author_sort Qiqi Xie
collection DOAJ
description 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.
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spelling doaj-art-7341b36df35d41798d06f7b9cb4cb5532025-08-20T03:41:40ZengNature Portfolionpj Precision Oncology2397-768X2025-03-019111410.1038/s41698-025-00829-5Multi-omics analysis identifies glioblastoma dependency on H3K9me3 methyltransferase activityQiqi Xie0Yuanning Du1Sugata Ghosh2Saranya Rajendran3Aaron A. Cohen-Gadol4José-Manuel Baizabal5Kenneth P. Nephew6Leng Han7Jia Shen8Medical Sciences Program, Indiana University School of MedicineMedical Sciences Program, Indiana University School of MedicineMedical Sciences Program, Indiana University School of MedicineMedical Sciences Program, Indiana University School of MedicineDepartment of Neurological Surgery, Indiana University School of MedicineDepartment of Biology, Indiana UniversityMedical Sciences Program, Indiana University School of MedicineBrown Center for Immunotherapy, Indiana University School of MedicineMedical Sciences Program, Indiana University School of MedicineAbstract 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.https://doi.org/10.1038/s41698-025-00829-5
spellingShingle Qiqi Xie
Yuanning Du
Sugata Ghosh
Saranya Rajendran
Aaron A. Cohen-Gadol
José-Manuel Baizabal
Kenneth P. Nephew
Leng Han
Jia Shen
Multi-omics analysis identifies glioblastoma dependency on H3K9me3 methyltransferase activity
npj Precision Oncology
title Multi-omics analysis identifies glioblastoma dependency on H3K9me3 methyltransferase activity
title_full Multi-omics analysis identifies glioblastoma dependency on H3K9me3 methyltransferase activity
title_fullStr Multi-omics analysis identifies glioblastoma dependency on H3K9me3 methyltransferase activity
title_full_unstemmed Multi-omics analysis identifies glioblastoma dependency on H3K9me3 methyltransferase activity
title_short Multi-omics analysis identifies glioblastoma dependency on H3K9me3 methyltransferase activity
title_sort multi omics analysis identifies glioblastoma dependency on h3k9me3 methyltransferase activity
url https://doi.org/10.1038/s41698-025-00829-5
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