Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

CLIC4 deficiency alters mitochondrial function and transcriptional profiles in murine breast cancer cells.

ABSTRACT: CLIC4 deficiency alters mitochondrial function and transcriptional profiles in murine breast cancer cells.

PROVIDER: PRJNA727829 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR14458837_1.fastq.gz	Fastqsanger.gz
	SRR14458837_2.fastq.gz	Fastqsanger.gz
	SRR14458838_1.fastq.gz	Fastqsanger.gz
	SRR14458838_2.fastq.gz	Fastqsanger.gz
	SRR14458839_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 30

Similar Datasets

CLIC4 deficiency alters mitochondrial function and transcriptional profiles in murine breast cancer cells.

Project description:We report the different transcriptom of 6DT1 (murine mammary cancer cell line) wildtype cells or CLIC4-KO (by CRISPR cas9) untreated or treated 1uM H2O2 for 24 hours.

2022-09-14 | GSE173997 | GEO

Host CLIC4 is essential for breast cancer metastatic competence

Project description:Chloride Intracellular Channel 4 (CLIC4) expression is elevated in the stroma of many cancers. We show that CLIC4 expression is higher in breast cancers from younger women and early stage metastatic disease, portends poor prognosis, and is linked to TGF-β expression. Two murine breast cancer models with lung metastases revealed that ablation of host Clic4 nearly eliminated lung metastases without reducing primary tumor size while Clic4 null tumor cells retained metastatic capability. Thus, CLIC4 is required for host metastatic competence. Deficiencies in circulating pro-metastatic soluble factors were detected in CLIC4 deficient hosts bearing primary tumors. Necrosis and vascular abnormalities were more abundant in primary tumors from CLIC4 deficient hosts than from CLIC4 proficient control hosts. Transcriptional profiles of lungs and primary tumors prior to the onset of metastases indicated that loss of host CLIC4 enhances an inflammatory microenvironment. Thus, CLIC4 expression in human breast cancers may serve as a prognostic biomarker, and targeting host CLIC4 could reduce metastatic competence.

2022-05-25 | GSE185163 | GEO

CLIC4 is essential for host competence for metastasis in murine models of breast cancer and a prognostic indicator for human breast cancer

Project description:CLIC4 belongs to a family of highly conserved metamorphic proteins of the glutathione‐S‐transferase superfamily and dysregulation is implicated in pulmonary arterial hypertension, asthma, and ovarian cancer. We show that genetic ablation of host Clic4 eliminated the establishment of breast cancer lung metastases in two independent mouse models while Clic4 null tumor cells retained metastatic capability. TCGA and METABRIC data indicated that CLIC4 is elevated in human breast cancers from young women, those with poor prognosis and those with early stage metastatic disease. Experimentally, the essential Clic4 host contributions for metastatic competence depended on circulating levels of pro‐ metastatic mediators, neoangiogenesis, tumor cell attachment to lung tissue, myofibroblast differentiation, and leukocyte migration. CLIC4 was abundant in circulating extracellular vesicles (EVs) from tumor‐bearing wildtype mice but absent in EVs from tumor‐bearing Clic4 null hosts or wildtype hosts bearing Clic4 null‐tumors suggesting cross‐talk between host and tumor cells is required to deposit CLIC4 in EVs. These results illuminate CLIC4 as a critical host factor for metastatic competence, a potential prognostic marker for breast cancer patients and a target for anti‐metastatic therapy.

2020-11-26 | GSE141057 | GEO

The oxidoreductase CLIC4 is required to maintain mitochondrial function and resistance to exogenous oxidants in breast cancer cells.

Project description:We report the different transcriptom of 6DT1 (murine mammary cancer cell line) wildtype cells or CLIC4-KO (by CRISPR cas9) untreated or treated 1uM H2O2 for 24 hours.

2022-07-15 | GSE188780 | GEO

TREM1 deficiency alters the tumor myeloid landscape

Project description:TREM1 deficiency alters the tumor myeloid landscape

| PRJEB65047 | ENA

Proteomics of CLIC4 overexpressing human pulmonary artery endothelial cells

Project description:To identify CLIC4 effectors by studying proteins expressiosn altered by CLIC4 overexpression in human pulmonary artery endothelial cells.

2018-10-16 | PXD008714 | Pride

Gene expression in the mitochondrial syndrome of coenzyme Q deficiency

Project description:Coenzyme Q10 deficiency syndrome includes a clinically heterogeneous group of mitochondrial diseases characterized by low content of CoQ10 in tissues. The only currently available treatment is supplementation with CoQ10, which improves the clinical phenotype in some patients but does not reverse established damage. Incubation with CoQ10 restored respiration and apoptotic pathways but did not affect lipid metabolism, cell growth, and undifferentiated phenotype presented by CoQ10 deficient cells. We conclude that the mitochondrial dysfunction caused byCoQ10 deficiency induces a stable survival adaptation of somatic cells from patients, thus explaining their incomplete recovery after treatment. We compared the gene expresion of human dermal fibroblast from healthy people (group 1) with fibroblast from diferent patient diagnosed with the human syndrome of coenzyme Q10 deficiency, which were treated (group 3) or not (group 2) with coenzyme Q10 to recovery ATP levels.

2013-04-05 | E-GEOD-33940 | biostudies-arrayexpress

CLIC4 interacting proteins - To identify proteins in human pulmonary artery endothelial cells that interact with CLIC4

Project description:To identify proteins in human pulmonary artery endothelial cells that interact with CLIC4

2018-10-16 | PXD008709 | Pride

Gene expression analysis in 13 patients with mitochondrial ATP synthase deficiency (Agilent)

Project description:Defects of mitochondrial functions lead in humans to vast array of usually multisystemic pathologies and several hundreds of diseases resulting from various defects of mitochondria biogenesis and maintenance, defects of respiratory chain complexes (OXPHOS) or defects of individual mitochondrial proteins are known. We used Agilent Whole Human Genome Microarray for gene expression profiling of genetically heterogeneous group of 13 patients with biochemically proven ATP synthase deficiency. Gene expression data analysis allowed classification of patients into several distinct groups, provided information on subgroup and patient specific gene expression profiles, defined candidate disease causing genes and gave basic information on pathogenic mechanisms associated with ATP synthase deficiency. Keywords: ATP synthase, mitochondrial biogenesis, ROS, gene expression, microarray, human Two-condition experiment, patients vs. controls cells. Biological replicates: 9 control, 13 patients, independently grown and harvested.

2008-08-01 | E-GEOD-10956 | biostudies-arrayexpress

Common gene expression profile in the mitochondrial syndrome of coenzyme Q deficiency

Project description:Coenzyme Q10 deficiency syndrome includes a clinically heterogeneous group of mitochondrial diseases characterized by low content of CoQ10 in tissues. The only currently available treatment is supplementation with CoQ10, which improves the clinical phenotype in some patients but does not reverse established damage. We analyzed the transcriptome profiles of fibroblasts from different patients irrespective of the genetic origin of the disease. These cells showed a survival genetic profile apt at maintaining growth and undifferentiated phenotype, promoting anti-apoptotic pathways, and favoring bioenergetics supported by glycolysis and low lipid metabolism. WE conclude that the mitochondrial dysfunction caused byCoQ10 deficiency induces a stable survival adaptation of somatic cells from patients. All samples in triplicate. We compare the gene expresion of human derman fibroblast to fibroblast from 4 different patient diagnosed with the human syndrome of coenzyme Q10 deficiency.

2013-04-05 | E-GEOD-33769 | 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