RNA N6-methyladenosine (m6A) regulates cell cycle progression in diffuse midline glioma (DMG) and confers sensitivity to FTO inhibition.
Overview
- School of Life and Environmental Sciences, University of Sydney, Sydney, NSW Australia
- Children’s Cancer Institute at Minderoo Children’s Comprehensive Cancer Centre, Sydney, NSW Australia
- School of Clinical Medicine, UNSW Sydney, Sydney, NSW Australia
- Kid’s Cancer Centre, Sydney Children’s Hospital, Randwick, NSW Australia
Abstract
Diffuse midline gliomas (DMG) are deadly pediatric brain cancers with limited treatment options. These tumors likely arise from oligodendrocyte precursor cells (OPC) that acquire a driver histone mutation, leading to an aberrant epigenome. RNA N6-methyladenosine (m6A) is a vital epi-transcriptomic modification that regulates RNA processes and plays a significant role in OPC development through its regulation of transcripts involved in histone modification processes. Despite this pivotal role in OPC biology, the epi-transcriptome has not yet been investigated in DMG, and its interrogation may uncover new therapeutic options and understanding of this disease. Therefore, for the first time, we generated base-resolution m6A landscapes for patient-derived DMG cultures and found that DMG exhibits elevated m6A levels compared to non-neoplastic patient cells, with particularly strong enrichment on transcripts involved in cell motility and migration. In contrast, the minority of transcripts that have lower levels of m6A in DMG were associated with cell cycle regulation, especially components of chromosome segregation machinery. We also demonstrate that DMG is sensitive to inhibition of the m6A demethylase FTO, with FB23-2 treatment resulting in decreased proliferation, reduced survival, and pronounced S-phase arrest/
Reproduced under the paper's license (CC BY), from the paper cited above.
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Data
Datasets cited
- geo:GSE279022, at NCBI GEO; found in “Data availability”
Data availability
Data generated in this study have been deposited to European Nucleotide Archive (ENA) under the accession PRJEB80588 and processed data at the Gene Expression Omnibus (GEO) under accession GSE279022 (https://
Reproduced under the paper's license (CC BY), from the paper cited above.
Versions
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Version 1, 30 September 2026: the first record
Recorded: type, language, journal, volume, issue, pages, dates, 7 authors, 4 keywords, 11 MeSH terms, 2 funders, 77 references.
Cite
This paper
Ross, S. E., Holliday, H., Wang, E., Zeraati, M., Tsoli, M., Ziegler, D. S., & Dinger, M. E. (2026). RNA N6-methyladenosine (m6A) regulates cell cycle progression in diffuse midline glioma (DMG) and confers sensitivity to FTO inhibition. Cell death & disease, 17(1), 371. https://
BibTeX
@article{ross2026rna,
author = {Ross, Samuel E and Holliday, Holly and Wang, Eyden and Zeraati, Mahdi and Tsoli, Maria and Ziegler, David S and Dinger, Marcel E},
title = {{RNA N6-methyladenosine (m6A) regulates cell cycle progression in diffuse midline glioma (DMG) and confers sensitivity to FTO inhibition}},
journal = {Cell death \& disease},
year = {2026},
month = mar,
volume = {17},
number = {1},
pages = {371},
publisher = {Nature Publishing Group},
issn = {2041-4889},
doi = {10.1038/
url = {https://
pmid = {41888518},
pmcid = {PMC13039948}
}
RIS
TY - JOUR
AU - Ross, Samuel E
AU - Holliday, Holly
AU - Wang, Eyden
AU - Zeraati, Mahdi
AU - Tsoli, Maria
AU - Ziegler, David S
AU - Dinger, Marcel E
TI - RNA N6-methyladenosine (m6A) regulates cell cycle progression in diffuse midline glioma (DMG) and confers sensitivity to FTO inhibition
T2 - Cell death & disease
J2 - Cell Death Dis
PY - 2026
DA - 2026/
VL - 17
IS - 1
SP - 371
SN - 2041-4889
PB - Nature Publishing Group
DO - 10.1038/
UR - https://
LA - en
ER -
CSL-JSON
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