Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

PRMT3-mediated cellular and molecular regulation in brain tumour stem cells.

ABSTRACT: Effect on gene expression profilng of BTSCs following PRMT3 inhibition with SGC707. To investigate the role of PRMT3 in regulating the cellular and molecular features of BTSCs, we performed RNA-seq using samples obtained from SGC707 treated versus XY1 treated GBM BTSCs.

ORGANISM(S): Homo sapiens

PROVIDER: GSE281186 | GEO | 2025/11/05

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

PRMT3 drives glioblastoma progression by enhancing HIF1A and glycolytic metabolism

Project description:To investigate the potential mechanisms underlying PRMT3 regulation of GBM growth, we performed RNA-seq transcriptomic profiling of U251 GBM cells treated with lenti-ShCtrl and shPRMT3.

2022-11-08 | GSE200902 | GEO

PRMT3-mediated cellular and molecular regulation in brain tumour stem cells.

Project description:PRMT3-mediated cellular and molecular regulation in brain tumour stem cells.

| PRJNA1182689 | ENA

Effect on gene expression profilng of BTSCs following HDAC1/2 inhibition with romidepsin.

Project description:To investigate the roles of HDAC1/2 in regulating the transcriptional programs associated with BTSC stem cell, growth and differentiation features, we performed RNA-seq using samples obtained from romidepsin treated versus DMSO vehicle treated GBM BTSCs.

2023-07-09 | GSE214721 | GEO

Effect of depletion of PRMT3 and IGF2BP1 on gene expression in PLC-8024 cells [PRMT3 IGF2BP1 KD RNA-seq]

Project description:To investigate the function PRMT3 and IGF2BP1 in HCC, we established PLC-8024 cell lines in which each target gene has been knocked down by shRNA.

2023-02-28 | GSE206502 | GEO

Asymmetrical methyltransferase PRMT3 regulates human mesenchymal stem cell osteogenesis via miR-3648

Project description:Histone arginine methylation, which is catalyzed by protein arginine methyltransferases (PRMTs), plays a key regulatory role in various biological processes, including signal transduction, RNA splicing, transcription and chromatin remodeling, and DNA repair. Several PRMTs are involved in skeletal development; however, their role in the osteogenic differentiation of mesenchymal stem cells (MSCs) is not completely clear. In this study, we aimed to elucidate the function of PRMT3, a type-I PRMT that catalyzes the formation of ω-mono- or asymmetric dimethyl arginine, in MSC osteogenesis. We found that PRMT3 is involved in MSC osteogenic commitment and bone remodeling. Then we did PRMT3 and H4R3me2a ChIP-seq in MSC to find the possible target genes.

2019-08-20 | GSE124674 | GEO

Targeting PRMT3 Impairs Methylation and Oligomerization of HSP60 to Boost Anti-Tumor Immunity by Activating cGAS/STING Signaling

Project description:Hepatocellular carcinoma (HCC) is a highly lethal cancer for which current available treatment options have limited efficacy. Immunotherapy has emerged as a promising therapeutic option for HCC, yet resistance to immunotherapy is a major challenge. Here, we uncover protein arginine methyltransferase 3 (PRMT3) as a novel driver of immunotherapy resistance in HCC. We show that PRMT3 expression is induced by activated T cells in response to immune checkpoint blockade (ICB) via an interferon-gamma (IFN)STAT1 signaling pathway, and that high PRMT3 expression inversely correlates with tumor-infiltrating CD8+ T cells and predicts poor response to ICB in HCC patients. We demonstrate that genetic depletion and pharmacological inhibition of PRMT3 induce a profound influx of T cells into tumors and activate anti-tumor immunity to suppress HCC progression. Mechanistically, we demonstrate that PRMT3 methylates HSP60, a mitochondrial chaperone protein, at R446, and that this novel post-translational modification is required for HSP60 oligomerization and maintaining mitochondrial homeostasis. We reveal that targeting PRMT3-dependent HSP60-R446 methylation boosts anti-tumor immunity by disrupting mitochondrial function, increasing mitochondrial DNA (mtDNA) leakage, and activating the cGAS/STING pathway, a key innate immune sensor of cytosolic DNA. Importantly, we provide genetic and pharmacologic evidence that targeting PRMT3 enhances anti-PD1 efficacy and anti-tumor immunity in HCC mouse models. Our study identifies PRMT3 as a potential biomarker and therapeutic target to overcome immunotherapy resistance in HCC.

2024-05-29 | GSE249999 | GEO

Genome-wide analysis of GBM-derived brain tumor stem cells-like (BTSCs)

Project description:Genome-wide analysis of GBM-derived brain tumor stem cells-like (BTSCs) collected at the Freiburg Medical Center and UAB (JX6)

2019-09-13 | GSE137310 | GEO

Transcriptional Control of Brain Tumour Stem Cells by a Carbohydrate Binding Protein

Project description:Brain tumour stem cells (BTSCs) and intratumoural heterogeneity represent major challenges in glioblastoma therapy. Here, we report that the LGALS1 gene, encoding the carbohydrate binding protein, galectin1, is a key regulator of BTSCs and glioblastoma resistance to therapy. Genetic deletion of LGALS1 alters BTSC gene expression profiles and results in downregulation of gene sets associated with mesenchymal subtype of glioblastoma. Using a combination of pharmacological and genetic approaches, we establish that inhibition of LGALS1 signalling in BTSCs impairs self-renewal, suppresses tumourigenesis, prolongs lifespan, and improves glioblastoma response to ionizing radiation in preclinical animal models. Mechanistically, we show that LGALS1 is a direct transcriptional target of STAT3 with its expression robustly regulated by the ligand OSM. Importantly, we establish that galectin1 forms a complex with the transcription factor HOXA5 to reprogram BTSC transcriptional landscape. Our data unravel an oncogenic signalling pathway by which galectin1/HOXA5 complex maintains BTSCs and promotes glioblastoma.

2021-08-31 | GSE180981 | GEO

Integrative and Quantitative Analysis of Tumor Progression Reveals Fundamental Properties of Glioblastoma

Project description:Principle of tumor growth is one fundamental aspect of cancer biology and it remains to be superficially understood. Here we developed a set of genetic and mathematic tools allow integrative analysis of mouse glioblastoma (GBM) progression. Quantitative temporal imaging of mouse GBM and mathematic modeling suggest that mouse GBM grows exponentially, which led to the discovery that a sustainable exponential growth requires outward migrating brain tumor stem cells (BTSCs). Quantitative single cell tracing of BTSCs in vivo unravels symmetric expansion of BTSCs, asymmetric differentiation, and a non-reversible differentiation process during tumor progression. Mosaic tracing of BTSCs and non-BTSCs reveals a cellular temporal dynamic changes and cellular turnover. These experimentally collected parameters were integrated step by step to a quantitative mathematic model of GBM growth, which faithfully predicts tumor cellular architecture, tumor response to chemotherapy and BTSC therapy. Bulk and single cell RNA-Seq reveals distinct molecular hierarchy and molecular heterogeneity in BTSCs, which was confirmed by analyzing human GBM single cell RNA-Seq results. This study reveals basic developmental principles that govern tumor development, which provides novel understanding of cancer development, tumor heterogeneity and new approaches to treat GBM.

2024-05-01 | GSE114456 | GEO

Integrative and Quantitative Analysis of Tumor Progression Reveals Fundamental Properties of Glioblastoma

Project description:The principle of tumor growth is one of the most fundamental aspects in cancer biology and it remains to be superficially understood. Here we developed a set of genetic and mathematical tools for integrative analysis of mouse glioblastoma (GBM) progression. Quantitative temporal imaging of mouse GBM and mathematical modeling suggest that mouse GBM grows exponentially, which led to the discovery that a sustainable exponential growth requires outward migrating brain tumor stem cells (BTSCs). Quantitative single cell tracing of BTSCs in vivo unravels symmetric expansion of BTSCs, asymmetric differentiation, and a non-reversible differentiation process during tumor progression. Mosaic tracing of BTSCs and non-BTSCs reveals cellular dynamic changes and turnover. These experimentally collected parameters were integrated step by step to a quantitative mathematical model of GBM growth, which faithfully predicts tumor cellular architecture, tumor response to chemotherapy and BTSC therapy. Bulk and single cell RNA-Seq reveals distinct molecular hierarchy and molecular heterogeneity in BTSCs, which was confirmed by analyzing human GBM single-cell RNA-Seq results. This study reveals fundamental developmental principles that govern tumor growth, which provides insights into understanding cancer development, tumor heterogeneity and GBM therapy.

2022-02-02 | GSE126212 | 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