Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Microglia promote glioblastoma growth via mTOR-mediated immunosuppressive conditioning of the tumor microenvironment.

ABSTRACT: Microglia promote glioblastoma growth via mTOR-mediated immunosuppressive conditioning of the tumor microenvironment.

PROVIDER: PRJNA613838 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR11363343_1.fastq.gz	Fastqsanger.gz
	SRR11363343_2.fastq.gz	Fastqsanger.gz
	SRR11363344_1.fastq.gz	Fastqsanger.gz
	SRR11363344_2.fastq.gz	Fastqsanger.gz
	SRR11363345_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 34

Similar Datasets

Microglia promote glioblastoma growth via mTOR-mediated immunosuppressive conditioning of the tumor microenvironment.

Project description:Tumor-associated microglia and macrophages (TAM) are the most numerous non-neoplastic populations in the tumor microenvironment of glioblastoma (GBM), the most common malignant brain tumor in adulthood. The mTOR pathway, an important regulator of cell survival and proliferation, is known to be upregulated in GBM, but little is known about a potential role of this pathway in TAM. Here, we show that GBM-initiating cells (GIC) induce mTOR signalling in TAM-Microglia (TAM-MG) but not TAM-Macrophages (TAM-BMDM) in in vitro and in vivo GBM mouse models. mTOR-dependent regulation of STAT3 and NF-ĸB activity promotes an immunosuppressed phenotype in TAM-MG which hinders effector T cell proliferation and immune reactivity, thereby contributing to tumor immune evasion and promoting tumor growth in a mouse model. The translational value of these results is demonstrated in whole transcriptome datasets of human GBM and in a novel in vitro model whereby IPSC-derived microglia-like cells are conditioned by syngeneic patient-derived GIC. These results raise the possibility that tumor cells might not be the primary target of mTOR inhibition, and TAM-MG should be considered instead.

2020-07-21 | GSE147329 | GEO

Immunosuppressive tumor microenvironment of osteosarcoma [scRNA-seq]

Project description:Immunosuppressive tumor microenvironment of osteosarcoma [scRNA-seq]

| PRJNA1272125 | ENA

Immunosuppressive tumor microenvironment of osteosarcoma [Spatial transcriptomics]

Project description:Immunosuppressive tumor microenvironment of osteosarcoma [Spatial transcriptomics]

| PRJNA1272124 | ENA

Multi-inlet spheroid generator for modeling immune microenvironment of glioblastoma (GBM)

Project description:Using the multi-inlet spheroid generator (MSG) platform, we generated stable GBM spheroids and observed their interactions with various immune cells, including microglia and natural killer (NK) cells, at different time points. HMO6 and NK-92 cells were used for microglia and NK cells, respectively. We examined the interactions between tumor-immune cells as well as between different immune cells. The generation of tri-cultured spheroids successfully recapitulated the immunosuppressive microenvironment of the GBM tumor.

2024-07-06 | GSE271170 | GEO

Adoptive Macrophages Suppress Glioblastoma Growth by Reversing Immunosuppressive Microenvironment through Programmed Phenotype Repolarization

Project description:Glioblastoma (GBM) is a highly lethal brain tumor resistant to immunotherapy due to poor drug brain delivery and an immunosuppressive microenvironment. This study introduces a macrophage-based adoptive cell therapy that reprograms the tumor immune landscape to suppress GBM growth. We reveal that macrophage homing to GBM is phenotype-dependent, with anti-inflammatory macrophages more efficiently navigating brain vasculature and targeting tumors. Based on this observatioin, we developed engineered M2-like macrophages (eM2-Mφs) capable of programmable polarization. These adoptive cells maintain an anti-inflammatory phenotype during early circulation, allowing deep tumor infiltration, and subsequently switch to a proinflammatory state within the tumor to trigger immune activation. Treatment with eM2-Mφs alone, or combined with low-dose irradiation and/or checkpoint inhibitor, remarkably suppressed tumor growth and extended survival in mouse models. This approach offers a promising strategy to overcome GBM’s immunosuppressive barriers and enhance immunotherapy efficacy

2025-09-04 | GSE306956 | GEO

Glucose-driven histone lactylation promotes the immunosuppressive activity of monocyte-derived macrophages in glioblastoma

Project description:Macrophages are critical components of the immunosuppressive microenvironment that restrict anti-cancer immunity in glioblastoma (GBM). However, how GBM shapes the regulatory function of macrophages remains elusive. Here, we report that monocyte-derived macrophages (MDM), but not yolk-sac derived microglia (MG), exhibited potent immunosuppressive activity, which was mediated by a population of glycolytic GLUT1+MDM, in an IL10-dependent manner. GBM-derived factors reprogrammed MDM towards glycolytic cells with enhanced avidity for glucose, which was mostly used to generate lactate. In turn, intracellular lactate caused lactylation of histone lysine residues that promoted MDM immunosuppressive activity via regulation of Il10 expression. GBM-primed activation of PERK supported glucose metabolism and regulated GLUT1 expression through ATF4 in MDM. PERK-deletion in MDM abrogated histone lactylation and suppressive activity, thereby promoting polyfunctional T cell-infiltration of tumors. In combination with immunotherapy, PERK-deletion blocked GBM progression. Our study demonstrates that glucose-driven histone lactylation controls MDM immunosuppressive function; all in a PERK-dependent manner.

2024-05-06 | GSE260700 | GEO

Immunosuppressive tumor microenvironment of osteosarcoma [Spatial transcriptomics]

Project description:Osteosarcoma is the most common malignant bone tumor in children, characterized by a high degree of genomic instability, resulting in copy-number alterations and genomic rearrangements without disease-defining recurrent mutations. Clinical trials based on molecular characterization have failed to find new effective therapies or improve outcomes over the last 40 years. To better understand the immune microenvironment of osteosarcoma, we performed single-cell RNA sequencing on six tumor biopsy samples, combined with a previously-published cohort of six samples. Additional osteosarcoma samples were profiled using spatial transcriptomics for validation of discovered subtypes and to add spatial context. Analysis revealed immunosuppressive cells, including myeloid-derived suppressor cells (MDSCs), regulatory and exhausted T-cells, and LAMP3+ dendritic cells. Using cell-cell communication modeling, we identified robust interactions between MDSCs and other cells, leading to NF-κB upregulation and an immunosuppressive microenvironment, as well as interactions involving regulatory T-cells and osteosarcoma cells that promoted tumor progression and a proangiogenic niche.

2025-07-15 | GSE299025 | GEO

Immunosuppressive tumor microenvironment of osteosarcoma [scRNA-seq]

2025-07-15 | GSE299023 | GEO

Microarray dataset of gene transcription in mouse microglia and peripheral monocytes in contextual fear conditioning

Project description:Using Illumina MouseWG-6v2 microarrays, we investigated the gene transcription changes in microglia and peripheral monocytes after contextual fear conditioning of C57BL/6J mice. Mice were trained with or without a single minimized footshock stimulation (0-s or 2-s, 0.4 mA) and re-exposed to the training context without footshock for three different durations 24 h later: 0 min (FS0), 3 min (FS3), or 30 min (FS30). Whole brain microglia and peripheral monocytes were prepared 24 h after re-exposure using a neural tissue dissociation kit, including non-footshock controls for two re-exposure durations (Con3 and Con30). The data can be valuable for researchers interested in glial cells and neurotransmission studies and are related to the research article “Contextual fear conditioning regulates synapse-related gene transcription in mouse microglia”.

2022-10-28 | E-MTAB-12361 | biostudies-arrayexpress

The Dual Role of CREPT in Glioblastoma: Promoting Proliferation and Shaping an Immunosuppressive Microenvironment through Chemo-MO and GZMK⁺ T Cell Interaction

Project description:Elevated CREPT promotes tumor cell proliferation and enhances CCL2 secretion, thereby recruiting Chemo-MOs. These Chemo-MOs then engage in regulatory interactions with GZMK+CD8+ T cells, suppressing T cell infiltration and ultimately establishing a robust immunosuppressive microenvironment.

2025-08-04 | GSE304176 | 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