Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Respones to treatment of H209 and H838 cell lines to treatment with the non-covalent inhibitor of TRXR1, DKFZ-608

ABSTRACT: DKFZ-608 induces oxidative stress in the cytoplasm of treated cancer cell lines. The molecular reason for this is the inhibition of the cytoplamic thioredoxin reductase TRXR1. The EC50 of cytotoxicity differes substantialy in SCLC (hypersensitive) and NSCLC (resistant). The experiment aims to identify stress response pathways induced by the compound which could explain the cytotoxic activity of the compound and its differential effect.

ORGANISM(S): Homo sapiens

PROVIDER: GSE123340 | GEO | 2019/12/02

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Respones to treatment of H209 and H838 cell lines to treatment with the non-covalent inhibitor of TRXR1, DKFZ-608

Project description:Respones to treatment of H209 and H838 cell lines to treatment with the non-covalent inhibitor of TRXR1, DKFZ-608

| PRJNA508383 | ENA

Expression data from U937 cells infected by hsa-miR-608 inhibitor virus

Project description:The expression level of miR-608 was found to be down regulated in several types of cancer. In our previous study, a single SNP in miR-608 (rs4919510) was found to be strongly associated with a higher risk of developing sepsis and multiple organ dysfunctions in all 3 independent study cohorts. However, the clinicopathological impact and the exact roles of miR-608 and its underlying molecular mechanisms in inflammation remain to be identified. In order to identify the exact terget gene of miR-608 in monocytes, we constructed lentiviral vectors with has-miR-608 inhibitor sequences and transfected U937 cells.We used microarrays to identified distinct classes of up-regulated genes during this process and look for possible target genes.

2015-12-12 | GSE75911 | GEO

Expression data from U937 cells infected by hsa-miR-608 inhibitor virus

2015-12-12 | E-GEOD-75911 | biostudies-arrayexpress

Inhibition of thioredoxin reductase 1 sensitizes glucose-starved glioblastoma cells to disulfidptosis 2

Project description:Disulfidptosis is a recently identified form of cell death characterized by the aberrant accumulation of cellular disulfides. This process primarily occurs in glucose-starved cells expressing higher levels of SLC7A11 and has been proposed as a therapeutic target for cancers with hyperactive SCL7A11. However, the potential for inducing disulfidptosis through other mechanisms in cancers remains unclear. Here, we found that inhibiting thioredoxin reductase 1 (TrxR1), a key enzyme in the thioredoxin system, induces disulfidptosis in glioblastoma (GBM) cells. TrxR1 expression is elevated in GBM with activated transcriptional coactivator with PDZ-binding motif (TAZ) and correlates with poor prognosis. TrxR1 inhibitors induced GBM cell death that can be rescued by disulfide reducers but not by ROS scavengers or inhibitors of apoptosis, ferroptosis, or necroptosis. Glucose-starved cells, but not those deprived of oxygen or glutamine, increased TrxR1 expression in an NRF2-dependent manner and were more sensitive to TrxR1 inhibition-induced cell death. The dying cells initially exhibited highly dynamic lamellipodia, followed by actin cytoskeleton collapse. This process involved the accumulation of cytosolic peroxisomes and micropinocytic caveolae, as well as small gaps in the plasma membrane. Depletion of the WAVE complex component NCKAP1 partially rescued the cells, whereas Rac inhibition enhanced cell death. In an orthotopic xenograft GBM mouse model, TrxR1 depletion inhibited tumor growth and improved survival. Furthermore, cells undergoing TrxR1 inhibition exhibited features of immunogenic cell death. Therefore, this study suggests the potential of targeting TrxR1 as a therapeutic strategy in GBM.

2024-12-23 | GSE282325 | GEO

Inhibition of thioredoxin reductase 1 sensitizes glucose-starved glioblastoma cells to disulfidptosis 3

2024-12-23 | GSE282334 | GEO

Inhibition of thioredoxin reductase 1 sensitizes glucose-starved glioblastoma cells to disulfidptosis 1

2024-12-23 | GSE282324 | GEO

Genome-wide analysis of the effects of the rs4919510C>G genotypes on the miRNA-608 target genes expression

Project description:Analysis of the effects of the rs4919510C>G SNP on miRNA-608 target gene expression. The hypothesis tested in the present study was that the rs4919510C>G SNP may influence the expression of miRNA-608 target genes. Results provide important information of the effects of the rs4919510C>G SNP on miRNA-608 target genes, including immunity and defense genes, DNA repair genes, cell growth-related genes, tumor invasion and metastasis-related genes, cancer stem cell-related genes, and cell death-related genes.

2013-05-15 | GSE46372 | GEO

Genome-wide analysis of the effects of the rs4919510C>G genotypes on the miRNA-608 target genes expression

2013-05-15 | E-GEOD-46372 | biostudies-arrayexpress

Campylobacter fetus subsp. venerealis 97/608

Project description:Campylobacter fetus subsp. venerealis 97/608 Genome sequencing

| PRJNA73807 | ENA

Genome-wide analysis of miR-552-3p- and miR-608-mediated gene silencing in A549 lung cancer cells

Project description:Analysis of changes in gene expression after transfection with miR-552-3p or miR-608 mimic in A549 cells Total RNA was obtained from A549 cells transfected with miR-552-3p or miR-608 or negative control mimic, and gene expression was compared using microarrays.

2015-12-15 | E-GEOD-62723 | biostudies-arrayexpress

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