Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNA-sequencing on sorted tumor-associated macrophages from vehicle or JHU083 pro-drug of 6-Diazo-5-oxo-L-norleucine (glutamine antagonist) treated 4T1 (breast cancer) tumor bearing mice

ABSTRACT: RNA-sequencing was performed on sorted tumor-associated macrophages (CD45+7AAD-CD11b+F4/80+CD8-Ly6C-Ly6G-) from 4T1 tumor (murine breast cancer) bearig mice with or without JHU083, pro-drug of 6-Diazo-5-oxo-L-norleucine (glutamine antagonist) treatment for expression profiling

ORGANISM(S): Mus musculus

PROVIDER: GSE119733 | GEO | 2020/07/08

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

RNA-sequencing on sorted infiltrating CD8 T cells from vehicle or JHU083, pro-drug of 6-Diazo-5-oxo-L-norleucine (glutamine antagonist) treated MC38 (colon cancer) tumor bearing mice

Project description:RNA-sequencing was performed on sorted CD11b-CD11c-B220-CD45+TCRbeta+CD44+CD8+ TIL from vehicle or JHU083 treated MC38 tumor-bearing mice with or without JHU083, pro-drug of 6-Diazo-5-oxo-L-norleucine (glutamine antagonist) treatment for expression profiling

2020-02-24 | GSE120345 | GEO

RNA-sequencing on sorted tumor-associated macrophages from vehicle or JHU083 pro-drug of 6-Diazo-5-oxo-L-norleucine (glutamine antagonist) treated 4T1 (breast cancer) tumor bearing mice

Project description:RNA-sequencing on sorted tumor-associated macrophages from vehicle or JHU083 pro-drug of 6-Diazo-5-oxo-L-norleucine (glutamine antagonist) treated 4T1 (breast cancer) tumor bearing mice

| PRJNA490152 | ENA

RNA-sequencing on sorted infiltrating CD8 T cells from vehicle or JHU083, pro-drug of 6-Diazo-5-oxo-L-norleucine (glutamine antagonist) treated MC38 (colon cancer) tumor bearing mice

Project description:RNA-sequencing on sorted infiltrating CD8 T cells from vehicle or JHU083, pro-drug of 6-Diazo-5-oxo-L-norleucine (glutamine antagonist) treated MC38 (colon cancer) tumor bearing mice

| PRJNA492801 | ENA

Combined with Gefitinib Overcomes Immunosuppression Induced by long-term Glutamine blockade in Bladder Cancer

Project description:Glutamine is a major energy source for tumor cells and blocking glutamine metabolism is being investigated as a promising strategy for cancer therapy. However, the antitumor effect of glutamine blockade in bladder cancer remains unclear, necessitating further investigation. Here, we demonstrated that glutamine metabolism was involved in the malignant progression of bladder cancer. Treatment with the glutamine antagonist 6-Diazo-5-oxo-L-norleucine (DON) inhibited bladder cancer cells in vitro in several ways. In addition, we observed a remarkable inhibition of tumor growth in bladder cancer-bearing mice using JHU083, a prodrug that was designed to prevent DON-induced toxicity. However, the antitumor immune effect of T cells changed from activation to inhibition as the administrated time extended. We found that both in vitro treatment with DON and in vivo prolonged administration of JHU083 led to the upregulation of PD-L1 in bladder cancer cells. Mechanistically, glutamine blockade up-regulates PD-L1 expression in bladder cancer cells by accumulating ROS, subsequently activating the EGFR/ERK/C-Jun signaling pathway. Combinatorial treatment with JHU083 and gefitinib reversed the up-regulation of PD-L1 in bladder cancer cells induced by prolonged glutamine blockade. This reversal resulted in the alleviation of T-cell immunosuppression and a significant improvement in therapeutic outcome. These preclinical findings suggested that broad targeting of glutamine metabolism could represent a viable therapeutic strategy for bladder cancer, with the potential for further enhancement through combined treatment with gefitinib.

2024-08-08 | GSE269520 | GEO

Glutamine antagonist JHU083 reprograms immunosuppressive tumor-associated macrophages to drive tumor immunity in urologic cancers, bulk RNA-seq

Project description:Glutamine metabolism in the tumor microenvironment is emerging as a critical regulator of immune-mediated anti-tumor responses. We report potent tumor growth inhibition by the glutamine antagonist prodrug JHU083 in urologic tumors by JHU083-reprogrammed tumor-associated macrophages (TAMs) and tumor-infiltrating monocytes (TIMs). Using orthogonal approaches, we show that JHU083-mediated glutamine antagonism in the tumor microenvironment induces TNF, inflammatory, and mTORC1 signaling in different intra-tumoral TAM clusters. Additionally, we report that JHU083 increases proliferation in tissue-resident macrophages intratumorally and in different TAM sub-clusters. Functionally, we report that JHU083-reprogrammed TAMs have increased tumor cell phagocytosis and diminished pro-angiogenic capacities. In vivo inhibition of glutamine consumption in TAMs results in increased glycolysis, broken TCA cycle, and disruption in purine metabolism. Although the effect of glutamine antagonism was less profound on tumor-infiltrating T cells for their anti-tumor activity, it promoted a stem cell-like phenotype in CD8+ T cells and decreased the CD4+ Treg abundance. Additionally, we report that JHU083 causes a global shutdown in glutamine utilizing metabolic pathways in tumor cells, leading to reduced HIF-1, c-MYC phosphorylation, and induction of tumor cell apoptosis, all key anti-tumoral features.

2024-05-18 | GSE229222 | GEO

Glutamine antagonist JHU083 reprograms immunosuppressive tumor-associated macrophages to drive tumor immunity in urologic cancers, single-cell RNA-seq

2024-05-18 | GSE229223 | GEO

Effect of rapamycin on murine subcutaneous MC38 tumor cell populations

Project description:To determine differential metabolic gene expression in distinct cell populations from subcutaneous MC38 tumors at baseline and in response to rapamycin, tumors from mice treated with vehicle or rapamycin were harvested, reconstituted to single cell suspensions, and flow sorted into cancer cell (CD45-), tumor-associated macrophage (TAM, CD45+ CD11b+ Ly6G- Ly6C lo F4/80 hi), monocytic myeloid-derived suppressor cell (M-MDSC, CD45+ CD11b+ Ly6G- Ly6C hi), CD8 T cell (CD45+ CD3+ CD8a+), and CD4 T cell (CD45+ CD3+ CD8a-) populations. RNA was extracted and transcripts were quantified by the NanoString nCounter Metabolic Pathways Panel.

2021-02-26 | GSE165223 | GEO

Heterogeneity of Ly6G+Ly6C+ myeloid-derived suppressor cell (MDSC) infiltrates during S. aureus biofilm infection

Project description:The two immune cell populations Myeloid-derived suppressor cells (MDSCs), monocytes (MONO) and neutrophils (PMNs) are difficult to differentiate because of shared surface marker expression. Here we utilize the integrin receptor CD11b combined with conventional Ly6G and Ly6C expression to more accurately separate cellular populations via FACS. Then we apply high-throughput RNA Sequencing to Ly6G+Ly6C+CD11bhigh MDSC, Ly6G+Ly6C+CD11blow PMN and Ly6G-Ly6C+ monocyte populations. A total of 6,466 genes were significantly differentially expressed in MDSCs vs. monocytes, whereas only 297 genes were significantly different between MDSCs and PMNs. A number of genes implicated in cell cycle regulation were identified, and in vivo EdU labeling revealed that over 75% of MDSCs proliferated locally at the site of S. aureus biofilm infection.

2018-10-03 | GSE118796 | GEO

Expression data from Ly6G+ and Ly6G- dendritic cells (DC)

Project description:To investigate the functional properties of Ly6G+ DC, we employed GeneChip analysis to compare the gene expression profiles between Ly6G+ DC and Ly6C- DC.

2013-02-01 | GSE28408 | GEO

Expression data from Ly6G+ and Ly6G- dendritic cells (DC)

Project description:To investigate the functional properties of Ly6G+ DC, we employed GeneChip analysis to compare the gene expression profiles between Ly6G+ DC and Ly6C- DC. Crude bone marrow (BM) cells prepared from C57BL/6 mice were cultured in the presence of GM-CSF. On day 6, CD11c+/MHC II+/Ly6G+ cells and CD11c+/MHC II+/Ly6G- cells were simultaneously sorted from the same cultures by FACSAria. Total RNA were extracted and hybridized on Affymetrix microarrays.

2013-02-01 | E-GEOD-28408 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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