Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The oncometabolite D-2HG alters T cell metabolism to impair CD8+ T cell function

ABSTRACT: The tumor-derived oncometabolite D-2HG impairs CD8+ T cell function through a novel metabolic target

ORGANISM(S): Mus musculus

PROVIDER: GSE209757 | GEO | 2022/09/01

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

The oncometabolite D-2HG alters T cell metabolism to impair CD8+ T cell function

Project description:The oncometabolite D-2HG alters T cell metabolism to impair CD8+ T cell function

| PRJNA862361 | ENA

Gene expression changes in hiPS-derived cardiomyocytes under R-2HG exposure and doxorubicin treatment

Project description:RNA sequencing and immunostaining in hiPS-derived cardiomyocytes indicated that the oncometabolite R-2HG exacerbated doxorubicin mediated cardiotoxicity.

2020-09-02 | GSE157282 | GEO

Transcriptome of human endothelial cells treated with R-2HG or S-2HG

Project description:Transcriptome profiling of human umbilical vein endothelial cells (HUVECs) treated with R-2HG or S-2HG to identify isomer-specific gene regulation.

2021-01-05 | GSE128633 | GEO

Gene expression profile of HCT116 and HT29 cells treated with D/L2HG

Project description:The oncometabolite, 2-hydroxyglutarate (2HG), has been directly implicated in carcinogenesis; however, the underlying molecular mechanisms remain poorly understood. To elucidate the molecular mechanisms through which 2HG contributes to cancer progression, we performed transcriptome analysis in 2HG-treated colorectal cancer HCT116 and HT29 cells.

2023-03-02 | GSE210167 | GEO

The anti-leukemic effect of R-2HG depends on its acting as an m6A mRNA modifier-RNA Seq-PBS / R-2HG treatment

Project description:RNA-seq from R-2HG sensitive leukemia cells treated with R-2HG or PBS.

2017-12-14 | GSE87189 | GEO

RNA-seq analysis after MIR4435-2HG knockdown in HemECs

Project description:Infantile hemangiomas (IHs) are commonly observed benign tumors that can cause serious complications.In this study, we investigated the role of M2 macrophage-derived exosomal lncRNA MIR4435-2HG in IHs. Exosomes derived from M2 polarized macrophages were extracted. Next, using cell co-culture or transfection, we investigated whether M2 polarized macrophage-derived exosomes (M2-exos) can transport MIR4435-2HG to regulate the proliferation, migration, invasion, and angiogenesis of hemangioma-derived endothelial cells (HemECs). RNA-seq and RNA pull-down assays were performed to identify targets and regulatory pathways of MIR4435-2HG. We explored the possible mechanisms through which MIR4435-2HG regulates the biological function of HemECs.We found that M2-exos significantly enhanced the proliferation, migration, invasion, and angiogenesis of HemECs. Thus, HemECs uptake M2-exos and promote biological functions through the inclusion of MIR4435-2HG. RNA-seq and RNA pull-down experiments confirmed that MIR4435-2HG regulates of HNRNPA1 expression and directly binds to HNRNPA1, consequently affecting the NF-κB signal pathway.In conclusion, MIR4435-2HG of M2-exos promotes the progression of IHs and enhances the proliferation, migration, invasion, and angiogenesis of HemECs by directly binding to HNRNPA1. This study not only reveals the mechanism of interaction between M2 macrophages and HemECs, but also provides a promising therapeutic target for IHs.

2023-10-29 | GSE236203 | GEO

Suppression of antitumor immunity by the oncometabolite 2-hydroxyglutarate

Project description:Isocitrate dehydrogenase (IDH) mutations, a hallmark of gliomagenesis, result in the production of the oncometabolite R-2-hydroxyglutarate (R-2-HG) which is thought to promote tumorigenesis via DNA methylation. Here we identify an additional immunosuppressive activity of R-2-HG: Tumor cell-derived R-2-HG is taken up by T-cells where it induces a strong and immediate perturbation of calcium- and ATP-dependent signaling events, and polyamine biosynthesis. This results in a profound suppression of antigen-specific T-cell activation and effector cytokine production in experimental mouse and human systems. In a large cohort of WHO grade II and III gliomas, IDH1 mutant tumors display reduced infiltration by T-cells compared to IDH1 wildtype tumors. Spontaneous and induced mutation-specific antitumor immunity to syngeneic IDH1-mutant tumors in MHC-humanized mice is improved by isolated genetic ablation of the neomorphic enzymatic function of mutant IDH1. Taken together, these data attribute a novel, fundamentally non-tumor-cell-autonomous role of an oncometabolite in shaping the tumor immune microenvironment. We investigated the effects of exogenous R-2-HG on primary human T cells.

2016-07-27 | E-GEOD-84849 | biostudies-arrayexpress

The effect of 2HG level on transcriptome at different stages of male mouse meiosis

Project description:We found that L2-hydroxyglutarate (2HG) level is 15 times higher in pachytene-diplotene (PD) stage as compared to leptotene-zygotene (LZ) stage. Since 2HG shows epigenetic effects we asked if the addition of 2HG to LZ cells or the decrease of 2HG level in PD cells will cause changes in gene expression.

2022-05-31 | GSE169014 | GEO

Transcriptome of human endothelial cells treated with R-2HG or S-2HG

Project description:Transcriptome of human endothelial cells treated with R-2HG or S-2HG

| PRJNA528313 | ENA

MIR4435-2HG as a novel predictive biomarker of chemotherapy response and death in pediatric B-cell ALL [methylation]

Project description:B-cell acute lymphoid leukemias (B-ALL) are the most common neoplastic diseases in children. Survival rates in Hispanics are lower than in non-Hispanic children. It is, therefore, necessary to find predictive and prognostic biomarkers of relapse and death in this population. Our aim was to identify biomarkers of treatment response, which may also predict relapse and death, through identifying differentially expressed and methylated genes between patients who responded or did not respond to induction treatment. DNA and RNA samples were extracted from 27 bone marrow samples from Hispanic children newly diagnosed with B-ALL. mRNA was sequenced using the NextSeq550 Illumina platform. Bisulfite-treated DNA was annealed to Illumina Infinium EPIC Methylation chips. Gene expression and differential methylation were compared between responders and non-responders at day 15 and at the end of induction chemotherapy. DAPK1, CNKSR3, MIR4435-HG2, CTHRC1, NPDC1, SLC45A3, ITGA6, and ASCL2 were overexpressed and hypomethylated in non-responders. The overexpression of MIR4435-2HG, DAPK1, ASCL2, SCL45A3, CNKSR3, and NPDC1 can predict non-response at day 15 and refractoriness. Additionally, higher expression of MIR4435-2HG increases the probability of non-response, death, and the risk of death. DAPK1, CNKSR3, and MIR4435-2HG are also overexpressed in relapse samples. Finally, MIR4435-2HG overexpression, together with positive minimal residual disease, is associated with poorer survival, and together with high expression of DAPK1 and ASCL2, it could improve the risk classification of patients with normal karyotype. In conclusion, MIR4435-2HG is a potential predictive biomarker in children with B-ALL, and its detection at diagnosis could improve survival rates in our patients.

2024-05-22 | GSE229052 | 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