Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNA N6-Methyladenosine (m6A) regulates cell cycle progression in Diffuse Midline Glioma (DMG) and confers sensitivity to FTO inhibition

ABSTRACT: The epitranscriptome has not previously been evaluated in DMG. Given the pivotal role of m6A in normal OPC biology, investigating its dysregulation in DMG could uncover new therapeutic options and improve our understanding of the disease's underlying mechanisms. Here, for the first time, we perform direct RNA-sequencing on patient-derived DMG cultures to generate transcript and base-resolution m6A landscapes of DMG. Furthermore, we interrogate the therapeutic benefits of the Fat mass and obesity associated (FTO) player inhibitor FB23-2 in DMG using direct RNA sequencing and RNA sequencing

ORGANISM(S): Homo sapiens

PROVIDER: GSE279022 | GEO | 2026/03/24

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

RNA N6-Methyladenosine (m6A) regulates cell cycle progression in Diffuse Midline Glioma (DMG) and confers sensitivity to FTO inhibition

Project description: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 improve our understanding of this disease. Therefore, for the first time, we generated base-resolution m6A landscapes for patient-derived DMG cultures and revealed a critical role in cell cycle regulation. We also find that DMG is sensitive to the inhibition of the m6A demethylase Fat Mass and Obesity Associated (FTO), with this inhibition leading to decreased survival and S-phase arrest/stress. Additionally, key cell cycle regulators, such as PLK1, are m6A-modified, contain YTHDF2 binding sites, and show significant changes following FTO inhibition on transcriptomic and proteomic levels. Collectively, these findings highlight the epi-transcriptome and its regulators as promising therapeutic targets for this currently uncurable disease.

2026-03-23 | PXD058793 | Pride

RNA N6-Methyladenosine (m6A) regulates the cell cycle in Diffuse Midline Glioma (DMG) and confers sensitivity to FTO inhibition

Project description:Direct RNA sequencing (m6A analysis) and RNA sequencing on DMG cultures after FTO inhibition via FB23-2 treatment

| PRJEB80588 | ENA

Histone H3 wild-type DIPG/DMG overexpressing EZHIP extend the spectrum diffuse midline gliomas with PRC2 inhibition beyond H3-K27M mutation

Project description:Characterisation of a new subgroup of DMG lacking H3-K27M mutation that is defined by H3K27me3 loss and EZHIP overexpression that can be detected by IHC. These tumors are distinct from EZHIP-positive posterior fossa ependymomas and are associated with a dismal prognosis. We propose that these EZHIP/H3-WT tumors need to be considered similar to canonical DIPG/DMG, thus extending the spectrum of DMG with PRC2 inhibition beyond H3-K27M mutation

2020-03-20 | E-MTAB-8888 | biostudies-arrayexpress

Analysis of m6A levels in K562 treted with the FTO inhibitor FB23-3 by m6A-mRNA&lncRNA Epitranscriptomic Microarray

Project description:FTO, an N6-methyladenosine demethylase, has emerged as a promising target for the treatment of specific acute myeloid leukemia (AML) subtypes. Here, we investigate the antiproliferative effects of the FTO inhibitor FB23-2 in leukemia. We demonstrate that FB23-2 potently inhibits proliferation across both AML and CML cell lines, irrespective of their responsiveness to FTO depletion. Interestingly, FB23-2 induces cell cycle arrest without a concurrent increase in m6A levels, suggesting an alternative mechanism of action.

2024-12-26 | GSE254577 | GEO

Targeting FTO suppresses hepatocellular carcinoma by inhibiting ERBB3 and TUBB4A expression [MeRIP]

Project description:Fat mass and obesity-associated protein (FTO) is an N6-methyladenosine (m6A) demethylase and plays a critical oncogenic role in various cancers. Here we show that FTO is an effective target in hepatocellular carcinoma (HCC). FTO is highly expressed in clinical patients of HCC and presents as a poor prognostic factor. Genetic depletion of FTO dramatically attenuated HCC progression in vivo. Pharmacological inhibition of FTO by FB23/FB23-2 remarkably suppressed the proliferation and migration of HCC cell lines in vitro, as well as inhibiting the HCC tumorigenicity in xeno-transplanted mice. Mechanistically, FB23-2 suppressed the expression of Erb-b2 receptor tyrosine kinase 3 (ERBB3) and human tubulin beta class Iva (TUBB4A) by increasing the m6A level in these mRNA transcripts. The decreased ERBB3 resulted in inhibited Akt-mTOR signaling that subsequently impaired the proliferation and survival of HCC cells. Moreover, FB23-2 abolished the organization of the tubulin cytoskeleton, while enforced expression of TUBB4A rescued the migration of HCC cells. Collectively, our study demonstrated that FTO plays a critical role in HCC by maintaining the proliferation and migration of cells, and highlights the broad potential of FTO inhibitors for targeting HCC.

2025-01-03 | GSE268330 | GEO

Targeting FTO suppresses hepatocellular carcinoma by inhibiting ERBB3 and TUBB4A expression [RNA-seq]

2025-01-03 | GSE268326 | GEO

Sequencing of mRNA with N6-methyladenosine (m6A) modification in AML cells upon DMSO or FTO inhibitor treatment

Project description:To identify the potential mRNA targets of FTO inhibitor, we conducted m6A-seq with mRNA samples enriched from AML cells upon DMSO and FB23-2 (FTO inhibitor) treatment

2019-04-29 | GSE103496 | GEO

DMG H3-K27M MAPK-altered methylation data

Project description:Diffuse midline gliomas (DMG) are aggressive tumors with a poor prognosis. In this study, a technique called t-SNE analysis was used to cluster tumors based on their methylation profiles. DMG subtype with a co-occurrence of H3.3K27M and BRAF or FGFR1 mutations have been identified. This subtype has a more favorable prognosis, with a median overall survival of 3 years.

2024-07-30 | E-MTAB-13471 | biostudies-arrayexpress

Generation of Syngeneic Orthotopic DMG Murine Models

Project description:Diffuse Midline Glioma (DMG) syngeneic orthotopic murine mouse models were used as high fidelity model of human DMG tumors as they recapitulate the heterogeneity, cell states and OncoTarget/OncoTreat drug predictions of human DMG tumors.

2025-12-22 | GSE262774 | GEO

The effects of FTO inhibitors on MeRIP-seq profiles in small cell lung cancer cell line

Project description:We reveal that pharmacological inhibition of fat mass and obesity-associated protein (FTO), a key m6A demethylase, exerts anti-tumor effects on the human small cell lung cancer (SCLC) cell line H69, with a close correlation to the remodeling of m6A modification landscape. We observed that FTO inhibitor treatment significantly elevates global m6A levels in H69 cells, which is attributed to the suppressed demethylase activity of FTO. Meanwhile, the FTO inhibitor FB23-2 can inhibit the proliferation of SCLC.

2026-01-01 | GSE314636 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data