Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Elevated ETV6 expression in glioma promotes an aggressive in vitro phenotype associated with shorter patient survival

ABSTRACT: Elevated ETV6 expression in glioma promotes an aggressive in vitro phenotype associated with shorter patient survival

PROVIDER: PRJNA648352 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Elevated ETV6 expression in glioma promotes an aggressive in vitro phenotype associated with shorter patient survival

Project description:Purpose It has been postulated that glioblastoma (GBM) has the ability to hijack neural progenitor migration mechanisms to facilitate tumor progression. Our previous data show that ETS variant 6 (ETV6) is highly expressed in human GBM and fetal astrocytes compared to normal mature astrocytes. We hypothesized that ETV6 played a role in GBM tumor progression. Methods Expression of ETV6 was first examined in 2 American and 3 Chinese tissue microarrays. The correlation between ETV6 staining intensity and patient survival was calculated, followed by validation using public databases-TCGA and REMBRANDT. The effect of ETV6 knockdown on glioma cell proliferation (EdU), viability (AnnexinV labeling), clonogenic growth (colony formation), and migration/invasion (transwell assays) in GBM cells was tested. RNA sequencing was performed to ellucidate the underlying molecular mechanisms. Results ETV6 was highly expressed in GBM and associated with an unfavorable prognosis. ETV6 silencing in glioma cells led to increased apoptosis and decreased proliferation, clonogenicity, migration, and invasion. RNA-Seq based gene expression and pathway analyses revealed that ETV6 knockdown in U251 cells led to the upregulation of genes involved in extracellular matrix organization, NF-κB signaling, TNFmediated signaling and downregulation of genes in regulation of cell motility, cell proliferation, PI3KAKT and Ras pathways. Conclusion Our findings suggested that ETV6 was highly expressed in GBM and its high expression correlated with poor survival. ETV6 silencing decreased an aggressive in vitro phenotype. The study encourages further investigation of ETV6 as a potential therapeutic target of GBM.

2021-01-01 | GSE155052 | GEO

Identification of ETV6 bound protein by affinity purification of ETV6-HA fusion protein in REH cells

Project description:To determine the protein partners of ETV6, we expressed ETV6 and HA-tagged ETV6 in Reh pre-B leukemic cells. Anti-HA magnetic beads were used for affinity purification of ETV6-HA (and ETV6 control) from the nuclear and cytoplasmic fraction. Following purification on-beads digest and LC-MS/MS experiments were performed at the Proteomics platform of the CHU de Quebec Research Center, Quebec, Canada.

2022-01-26 | PXD031001 | Pride

ETV6-NCOA2 expression profile in T/M mixed-phenotype acute leukemia [ETV6-NCOA2 human]

Project description:Exparession profiling of ETV6-NCOA2 at different stages of disease dEmpty vectorelopment: CD34 cord blood cells transduced with ETV6-NCOA2-GFP or with empty vector-GFP, CD34 cord blood cells transduced with ETV6-NCOA2-NGFR or ETV6-NCOA2-NGFR + NOTCH1-L1601PdP-GFP and transplanted in NSGS mice, and ETV6-NCOA2 patient derived xenografts.

2022-05-16 | GSE161702 | GEO

ChIP sequencing of ETV6-NCOA2 H3K27Ac profile in T/M mixed-phenotype acute leukemia

Project description:H3K27Ac ChIP-sequencing of CD34 positive cord blood cells expressing either ETV6-NCOA2 or empty-vector in-vitro and ETV6-NCOA2 patient derived xenograft.

2022-05-16 | GSE161624 | GEO

ETV6-NCOA2 expression profile in T/M mixed-phenotype acute leukemia [ETV6_NCOA2_Mouse_in_vitro]

Project description:Exparession profiling of lineage negative bone marrow cells from C57B/6 mice expressing either ETV6-NCOA2, KAT6-NCOA2 or empty-vector after five days in in-vitro culture.

2022-05-16 | GSE161703 | GEO

ETV6-NCOA2 expression profile in T/M mixed-phenotype acute leukemia [ETV6-NCOA2 human]

Project description:ETV6-NCOA2 expression profile in T/M mixed-phenotype acute leukemia [ETV6-NCOA2 human]

| PRJNA679212 | ENA

ChIP-seq for RUNX1 and ETV6-RUNX1 in an induced pluripotent stem cell model of ETV6-RUNX1 pre-leukaemia

Project description:ETV6-RUNX1 is a first-hit mutation in childhood B cell precursor acute lymphoblastic leukaemia. ETV6-RUNX1 is a fusion protein which inherits the DNA-binding runt domain from RUNX1. Here we performed chromatin precipitation for native RUNX1 and ETV6-RUNX1 using RUNX1 antibodies and specifically for the ETV6-RUNX1 fusion using a V5-tag pull down.

2022-10-31 | E-MTAB-12208 | biostudies-arrayexpress

Genome wide mapping of ETV6 binding sites in pre-B leukemic cells

Project description:Background: Genetic alterations in the transcriptional repressor ETV6 are associated with hematological malignancies. Notably, the t(12;21) translocation leading to an ETV6-AML1 fusion gene is the most common genetic alteration found in childhood acute lymphoblastic leukemia. Moreover, most of these patients also lack ETV6 expression, suggesting a tumor suppressor function. Results: To gain insights on ETV6 DNA-binding specificity and genome wide transcriptional regulation capacities, we performed chromatin immunoprecipitation experiments coupled to deep sequencing in a t(12;21)-positive pre-B leukemic cell line. This strategy led to high quality ETV6-bound regions. ETV6 binding is mostly cell type-specific as only few regions are shared with other blood cell subtypes. Peaks localization and motif enrichment analyses revealed a unique binding profile that is associated with the presence of the ETV6-AML1 fusion product. Conclusions: We described the first ETV6 binding map in the t(12;21) background. This study highlighted the complex and unique interplay between ETV6 and ETV6-AML1 and underscored the highly regulated mechanisms of ETV6 binding. ETV6 inactivation observed in this context could induce specific transcriptional changes promoting leukemic transformation.

2017-11-15 | GSE102785 | GEO

Identification of ETV6/RUNX1 regulated lncRNAs

Project description:Overwhelming evidence indicates that long non-coding RNAs have essential roles in tumorigenesis. Nevertheless, their expression and role in pediatric B-cell precursor acute lymphoblastic leukemia has not been extensively explored. Here, we conducted a comprehensive analysis of the long non-coding RNA transcriptome in ETV6/RUNX1 positive BCP-ALL, one of the most frequent subtypes of pediatric leukemia. An ETV6/RUNX1 expression signature was established, consisting of 596 lncRNAs (434 up and 162 down) using expression analysis of a series of primary patient samples. Subsequently, RNA sequencing from BCP-ALL cell lines and shRNA-mediated silencing of ETV6/RUNX1, illustrated that lnc-NKX2-3-1, lnc-TIMM21-5, lnc-ASTN1-1 and lnc-RTN4R-1 are bona fide ETV6/RUNX1 targets and could serve as novel biomarkers of this prevalent subtype of human leukemia.

2016-09-26 | GSE79868 | GEO

ETV6 Deficiency and Microsatellite Enhancers Drive Transcriptional Dysregulation in B-Lymphoblastic Leukemia: RNA-Seq

Project description:Distal enhancers play critical roles in sustaining oncogenic gene expression programs. We obtained ATAC-Seq data and ChIP-Seq data using antibodies against the H3K27ac histone mark, transcription factors ERG and ETV6, and input chromatin from B-ALL cell lines and comparator B-cell cancer cell lines, including B-ALL with biallelic ETV6 inactivation, ETV6-RUNX1, and intact ETV6. We identify aberrant enhancer-like activation of GGAA tandem repeats as a characteristic feature of B-cell acute lymphoblastic leukemia (B-ALL) with genetic defects of the ETV6 transcriptional repressor, including ETV6-RUNX1+ and ETV6-null B-ALL. We show that GGAA repeat enhancers are direct activators of previously identified ETV6-RUNX1+ B-ALL “signature” genes, including likely oncogenic drivers. When restored to ETV6-deficient B-ALL cells, ETV6 directly binds to GGAA repeat enhancers, represses their acetylation, downregulates adjacent genes, and inhibits B-ALL growth. In ETV6-deficient B-ALL cells, we find that the ETS transcription factor ERG directly binds to GGAA microsatellite enhancers and is required for sustained activation of many repeat enhancer-activated genes. Together, our findings reveal a novel epigenetic gatekeeper function of the ETV6 tumor suppressor gene and establish microsatellite enhancers as a key mechanism underlying the unique gene expression program of ETV6-RUNX1+ B-ALL.

2022-10-23 | GSE186936 | GEO

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