Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

SUV39H1 inhibition by Chaetocin targets stemness and oncogenic networks and synergizes with ONC201 against Diffuse intrinsic pontine gliomas [RNA-seq]

ABSTRACT: To investigate Chaetocin impact on Diffuse intrinsic pontine gliomas treatment We then performed gene expression profiling analysis using data obtained from RNA-seq of Chaetocin treatment and SUV39H1 knockdown in SU-DIPG36 cells

ORGANISM(S): Homo sapiens

PROVIDER: GSE225027 | GEO | 2025/02/08

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

SUV39H1 inhibition by Chaetocin targets stemness and oncogenic networks and synergizes with ONC201 against Diffuse intrinsic pontine gliomas [CUT&RUN]

Project description:To identify potential direct targets of SUV39H1, we performed Cut&Run-seq for H3K9me3 and SUV39H1 genomic occupancy

2025-02-08 | GSE225028 | GEO

SUV39H1 inhibition by Chaetocin targets stemness and oncogenic networks and synergizes with ONC201 against Diffuse intrinsic pontine gliomas

Project description:SUV39H1 inhibition by Chaetocin targets stemness and oncogenic networks and synergizes with ONC201 against Diffuse intrinsic pontine gliomas

| PRJNA933586 | ENA

SUV39H1 inhibition by Chaetocin targets stemness and oncogenic networks and synergizes with ONC201 against Diffuse intrinsic pontine gliomas [CUT&RUN]

Project description:SUV39H1 inhibition by Chaetocin targets stemness and oncogenic networks and synergizes with ONC201 against Diffuse intrinsic pontine gliomas [CUT&RUN]

| PRJNA934586 | ENA

SUV39H1 inhibition by Chaetocin targets stemness and oncogenic networks and synergizes with ONC201 against Diffuse intrinsic pontine gliomas [RNA-seq]

Project description:SUV39H1 inhibition by Chaetocin targets stemness and oncogenic networks and synergizes with ONC201 against Diffuse intrinsic pontine gliomas [RNA-seq]

| PRJNA934587 | ENA

SUV39H1 inhibition by Chaetocin targets stemness and oncogenic networks and synergizes with ONC201 against Diffuse intrinsic pontine gliomas

Project description:This SuperSeries is composed of the SubSeries listed below.

2025-02-08 | GSE225029 | GEO

SUV39H1 epigenetically modulates the MCPIP1-AURKA signaling axis to enhance neuroblastoma tumorigenesis

Project description:Epigenetic regulation is a pivotal factor during neuroblastoma (NB) pathogenesis and investigations into cancer epigenetics are actively underway to identify novel therapeutic strategies for NB patients. SUV39H1, a member of the H3K9 methyltransferase family, contributing to tumorigenesis across multiple malignancies. However, its specific role in NB remains unexplored. In this study, we conducted a high-throughput screen utilizing a compound library containing 288 epigenetic drugs, leading to the identification of chaetocin as the most potent NB inhibitor by targeting SUV39H1. Genetic manipulation and therapeutic inhibition of SUV39H1 significantly impacted proliferation, migration, cell cycle phases, and apoptosis in NB cells. Concurrently, chaetocin demonstrated robust anti-tumor efficacy in vivo with tolerable toxicity. RNA-seq unveiled that SUV39H1 knockdown and inhibition down-regulated cell cycle pathways, impacting vital genes such as AURKA. Besides, MCPIP1 emerged as a novel tumor suppressor following SUV39H1 inhibition, which decreased AURKA expression in NB. In detail, SUV39H1 mediated the enrichment of H3K9me3 at the promoter region of MCPIP1, repressing the MCPIP1-mediated degradation of AURKA and facilitating the subsequent accumulation of AURKA, which revealed the oncogenic role of SUV39H1 via the SUV39H1-MCPIP1-AURKA signaling axis in NB. Therapeutic inhibition of SUV39H1 using chaetocin emerges as an effective and safe strategy for NB patients.

2024-12-10 | GSE254118 | GEO

Chaetocin efficacy on Dahl rat

Project description:Transcriptional profiling of left ventricular tissues of Dahl rat with or without treatment of chaetocin Three-condition experiment, Control vs. failing heart, failing heart vs. treatment with chaetocin. 3 samples mixture per each group

2016-04-01 | E-GEOD-66617 | biostudies-arrayexpress

SUV39H1 Maintains Cancer Stem Cells in Glioblastoma [RNA-seq]

Project description:Glioblastoma (GBM) is the deadliest brain cancer, driven in part by GBM stem cells (GSCs) that contribute to therapeutic resistance and tumor recurrence. Effective targeting and elimination of GSCs hold promise for preventing GBM recurrence and achieving potential cures. In this study, we explored the role of the epigenetic regulator SUV39H1 in GSC maintenance and GBM progression. We observed that SUV39H1 is upregulated in GBM samples compared to normal brain tissues. Single-cell RNA-seq data indicated that SUV39H1 is preferentially expressed in GSCs relative to non-stem GBM cells, possibly due to super-enhancer-mediated transcriptional activation. Knockdown of SUV39H1 in patient-derived GSCs impaired their proliferation and stemness. RNA-seq analysis revealed that SUV39H1 regulates G2/M cell cycle progression, stem cell maintenance, and cell death pathways in GSCs. Integrated ATAC-seq (assay for transposase-accessible chromatin followed by sequencing) and RNA-seq analyses demonstrated that targeting SUV39H1 altered chromatin accessibility in key genes associated with these pathways. Treatment with chaetocin, a SUV39H1 inhibitor, mimicked the effects of SUV39H1 knockdown in GSCs and sensitized them to the GBM chemotherapy drug temozolomide (TMZ). In vivo studies using an intracranial patient-derived xenograft model showed that targeting SUV39H1 inhibited GSC-driven tumor formation in mice. Our findings identify SUV39H1 as a critical regulator of GSC maintenance and suggest that targeting SUV39H1 could disrupt GSCs and enhance the efficacy of existing chemotherapy, offering a promising strategy for improving GBM treatment outcomes.

2024-11-06 | GSE273012 | GEO

SUV39H1 Maintains Cancer Stem Cells in Glioblastoma [ATAC-seq]

2024-11-06 | GSE273013 | GEO

Genome-wide Analyses of Diffuse Intrinsic Pontine Gliomas

Project description:Purpose: More than 90% of children with diffuse intrinsic pontine glioma (DIPG) die within 2 years of diagnosis. There is a dire need to identify therapeutic targets, however lack of patient material for research has limited progress. We evaluated a large cohort of diffuse intrinsic pontine gliomas (DIPGs) to identify recurrent genomic abnormalities and gene expression signatures underlying DIPG. Patients and Methods: We used single nucleotide polymorphism arrays to evaluate genomic copy number imbalances in 43 DIPGs from 40 patients and in 8 low-grade exophytic brainstem gliomas. Gene expression arrays were used to evaluate expression signatures from 27 DIPGs, 6 low-grade exophytic brainstem gliomas and 66 low-grade gliomas arising outside the brainstem. Results: Frequencies of specific large-scale and focal imbalances varied significantly between DIPGs and pediatric glioblastomas outside the brainstem. Focal amplifications of genes within the receptor tyrosine kinase-Ras-PI3-kinase signaling pathway were found in 47% of DIPG, with PDGFRA and MET showing the highest frequency. 30% of DIPG contained focal amplifications of cell-cycle regulatory genes controlling RB phosphorylation, and 21% had concurrent amplification of genes from both pathways. Some tumors showed heterogeneity in amplification patterns. DIPGs showed distinct gene expression signatures relating to developmental processes compared to pediatric glioblastomas arising outside the brainstem, while expression signatures of low-grade exophytic brainstem gliomas were similar to low-grade gliomas outside the brainstem. Copy number analaysis: 43 DIPG samples, 8 Low Grade Gliomas using SNP6.0. Available matched normals are also profiled with SNP6.0. Expression analysis: 29 DIPG samples, 6 Low grade samples Please contact Suzanne Baker at Suzanne.Baker@stjude.org for CEL files and genotype calls.

2011-09-20 | E-GEOD-26576 | biostudies-arrayexpress

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