Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

PRMT3 drives glioblastoma progression by enhancing HIF1A and glycolytic metabolism

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE200902 | GEO | 2022/11/08

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:Glioblastoma (GBM) is the most common and aggressive primary brain tumor, but the mechanisms underlying tumor growth and progression remain unclear. The protein arginine methyltransferases (PRMTs) regulate a variety of biological processes, however, their roles in GBM growth and progression are not fully understood. In this study, our functional analysis of gene expression networks revealed that among the PRMT family expression of PRMT3 was most significantly enriched in both GBM and low-grade gliomas. Higher PRMT3 expression predicted poorer overall survival rate in patients with gliomas. Knockdown of PRMT3 markedly reduced the proliferation and migration of GBM cell lines and patient-derived glioblastoma stem cells (GSC) in cell culture, while its over-expression increased the proliferative capacity of GSC cells by promoting cell cycle progression. Consistently, stable PRMT3 knockdown strongly inhibited tumor growth in xenograft mouse models, along with a significant decrease in cell proliferation as well as an increase in apoptosis. We further found that PRMT3 reprogrammed metabolic pathways to promote GSC growth via increasing glycolysis and its critical transcriptional regulator HIF1α. In addition, pharmacological inhibition of PRMT3 with a PRMT3-specific inhibitor SGC707 impaired the growth of GBM cells. Thus, our study demonstrates that PRMT3 promotes GBM progression by enhancing HIF1A-mediated glycolysis and metabolic rewiring, presenting a point of metabolic vulnerability for therapeutic targeting in malignant gliomas.

| S-EPMC9646854 | biostudies-literature

PRMT3 drives glioblastoma progression by enhancing HIF1A and glycolytic metabolism

Project description:PRMT3 drives glioblastoma progression by enhancing HIF1A and glycolytic metabolism

| PRJNA827164 | ENA

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

Project description: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.

2025-11-05 | GSE281186 | 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

Expression data from U251-shCtrl and U251-shCPVL cells

Project description:we performed microarray expression profiling to analyze the differentially expressed genes between U251-shCtrl and U251-shCPVL cells.

2024-11-01 | GSE188414 | GEO

Study on the effects of CD44 knockdown in glioblastoma multiforme cells in combination with Temozolomide

Project description:Our goal is to investigate the effects of CD44 knockdown alone and in combination with Temozolomide on glioblastoma multiforme cells. To achieve this, we treated U251 cells that had been transfected with either shCtrl lentivirus or shCD44 lentivirus with either DMSO or Temozolomide.

2023-08-31 | GSE225869 | GEO

Gene based expression changes in glioblastoma cells after downregulation of MPS1 kinase

Project description:Gene expression changes were analyzed in U251 GBM cells after downregulation of MPS1 by RNA interference technology at different time points Microarray analysis was used to compare the mRNA expression profile of siMPS1 silenced U251 cells compared to siNegative (siNeg) and untransfected (Control) cells at 6, 24 and 48 hours post tranfection

2015-06-15 | E-GEOD-57091 | biostudies-arrayexpress

Chronic IFN-γ Exposure Drives Divergent Cellular and Molecular Responses in Glioblastoma Subtypes

Project description:Background: Glioblastoma (GBM) is an aggressive primary brain tumor with poor prognosis and limited treatments. Interferon-gamma (IFN-γ) plays a complex role in modulating immune and tumor responses, and its long-term impact on GBM remains unclear. Methods: Human GBM cell lines U87 and U251 were subjected to up to 28 days of chronic IFN-γ exposure and assessed for morphology, gene expression, protein dynamics, and cytokine secretion. RNA sequencing, automated Western blotting, and single-cell proteomics were employed to uncover distinct cellular and molecular adaptations to prolonged IFN-γ signaling. Results: Chronic IFN-γ exposure induced significantly divergent phenotypic changes in U87 and U251 cells. U87 cells formed neurosphere-like structures and upregulated STAT1/STAT3 signaling, suggesting an immunogenic response. In contrast, U251 cells displayed elongated morphologies and activated PI3K-Akt and Erk pathways, promoting survival and immune evasion. Differential gene expression analysis highlighted unique temporal profiles, with U251 cells exhibiting higher expression of immune resistance genes such as PD-L1 and VEGF. Secretome profiling further demonstrated contrasting cytokine landscapes: U87 cells secreted pro-inflammatory cytokines, while U251 cells produced immunosuppressive factors. Conclusions: Chronic IFN-γ exposure drives distinct molecular and phenotypic changes in GBM subtypes, reflecting their intrinsic heterogeneity. While IFN-γ enhances immune activation, prolonged exposure may also promote immune escape. These findings emphasize the need for therapeutic strategies combining IFN-γ with immune checkpoint inhibitors and targeted pathway modulation to optimize GBM treatment outcomes.

2025-08-12 | GSE304761 | 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