Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Genome wide chromatin changes in TC-32 and TC-71 Ewing sarcoma cell lines.

ABSTRACT: We performed ChIPseq on histone modification marks, transcriptional factors and chromatin architectural proteins in TC-32 and TC-71 Ewing sarcoma cell lines.

ORGANISM(S): Homo sapiens

PROVIDER: GSE115250 | GEO | 2019/08/07

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Genome wide chromatin changes in TC-32 and TC-71 Ewing sarcoma cell lines.

Project description:Genome wide chromatin changes in TC-32 and TC-71 Ewing sarcoma cell lines.

| PRJNA474339 | ENA

Gene expression of two Ewing sarcoma cell lines (SK-N-MC, TC-71), transfected with inducible re-expression of TCF7L1 or Empty control

Project description:This dataset comprises trnscriptome data of two Ewing sarcoma cell lines (SK-N-MC and TC-71) after re-expression of the gene TCF7L1

2022-01-11 | GSE165929 | GEO

Gene expression and exon splicing of two Ewing sarcoma cell lines (TC-32, RDES), transiently transfected with shControl or two different shRNA against SOX6

Project description:In this dataset, we include the gene expression and exon splicing variants of two Ewing sarcoma cell lines (RDES and TC-32) after knockdown of the transcription factor SOX6 in order to obtain differentially expressed genes and different exon splicing variants.

2020-04-01 | GSE120576 | GEO

EWS TC-71 cell lines: IGF-1R resistant

Project description:Ewing's Sarcoma cell lines were made resistant to different IGF-1R drugs to investigate mechanisms and pathways modulated by the resistance. EWS TC-71 cell line was exposed to increasing concentration to three different anti-IGF-1R drugs (HAb AVE1642, TKI NVP-AEW541, HAb CP-751,871, cell lines named respectively as TC/AVE, TC/AEW or TC/CP) for at least six months. Expression profile of resistant cell variants was compared either singularly for each resistance or commonly vs. parental cell line. Two technical replicates for resistant variants and three biological replicated for parental cell were present.

2012-10-03 | E-GEOD-34027 | biostudies-arrayexpress

Exosomes from CD99-deprived Ewing sarcoma cells reverse tumor malignancy

Project description:We evaluated the miRNA content of CD99pos EXOs isolated from the parental cell line TC-71 (three samples) and of CD99neg EXOs isolated from TC-CD99-shRNA cells (four samples) by microarray analysis.

2019-07-01 | E-MTAB-7585 | biostudies-arrayexpress

Novel targeting of DNA methyltransferase activity inhibits Ewing sarcoma cell proliferation and enhances tumor cell sensitivity to DNA damaging drugs by activating the DNA damage response

Project description:Genome wide epigenomic analysis of Ewing Sarcoma human cell lines treated with 5AzadC and MC3343. Samples included 9 x TC-71, 9 x A673 samples, and 8 x PDX samples. For each cell line and condition ( 5AzadC, MC3343, Contol), we created 3 replicates, except PDX with 5AzadC treatment for which only 2 samples were created.

2022-06-01 | GSE202143 | GEO

Targeting the EWS/ETS transcriptional program by BET bromodomain inhibition in Ewing sarcoma

Project description:Ewing sarcomas (ES) are highly malignant, osteolytic bone or soft tissue tumors, which are characterized by early metastasis into lung and bone. Genetically, ES are defined by balanced chromosomal EWS/ETS translocations, which give rise to chimeric proteins (EWS-ETS) that generate an oncogenic transcriptional program associated with altered epigenetic marks throughout the genome. By use of an inhibitor (JQ1) blocking BET bromodomain binding proteins (BRDs) we strikingly observed a strong down-regulation of the predominant EWS-ETS protein EWS/FLI1 in a dose dependent manner. Microarray analysis further revealed JQ1 treatment to block a typical ES associated expression program. The effect on this expression program could be mimicked by RNA interference with BRD3 or BRD4 expression, indicating that the EWS/FLI1 mediated expression profile is at least in part mediated via such epigenetic readers. Consequently, contact dependent and independent proliferation of different ES lines was strongly inhibited. Mechanistically, treatment of ES resulted in a partial arrest of the cell cycle as well as induction of apoptosis. Tumor development was suppressed dose dependently in a xeno-transplant model in immune deficient mice, overall indicating that ES may be susceptible to treatment with epigenetic inhibitors blocking BET bromodomain activity and the associated pathognomonic EWS-ETS transcriptional program in ES. Ewing sarcoma cell lines A673 and TC-71 were treated for 48 hours with 2 microM JQ1 or DMSO control.

2015-12-08 | E-GEOD-72673 | biostudies-arrayexpress

Gene expression of two Ewing sarcoma cell lines (SK-N-MC, TC-71), transfected with inducible re-expression of TCF7L1 or Empty control

Project description:Gene expression of two Ewing sarcoma cell lines (SK-N-MC, TC-71), transfected with inducible re-expression of TCF7L1 or Empty control

| PRJNA698592 | ENA

Ewing Sarcoma

Project description:This SuperSeries is composed of the following subset Series: GSE36857: Goldengate Methylation analysis: Ewing Sarcoma GSE36858: 5- AZA treatment of EWS cell lines Refer to individual Series

2012-09-01 | E-GEOD-36859 | biostudies-arrayexpress

Transcription profiling of human Ewing sarcoma samples and EWS-FLI-1 inhibited Ewing sarcoma cell lines

Project description:The cellular origin of Ewing tumor (ET), a tumor of bone or soft tissues characterized by specific fusions between EWS and ETS genes, is highly debated. Through gene expression analysis comparing ETs with a variety of normal tissues, we show that the profiles of different EWS-FLI1-silenced Ewing cell lines converge toward that of mesenchymal stem cells (MSC). Moreover, upon EWS-FLI1 silencing, two different Ewing cell lines can differentiate along the adipogenic lineage when incubated in appropriate differentiation cocktails. In addition, Ewing cells can also differentiate along the osteogenic lineage upon long-term inhibition of EWS-FLI1. These in silico and experimental data strongly suggest that the inhibition of EWS-FLI1 may allow Ewing cells to recover the phenotype of their MSC progenitor. Experiment Overall Design: Ewing tumors and EWS-FLI-1 inhibited cell lines were profiled on Affymetrix U133A (GPL96) arrays.

2008-06-15 | E-GEOD-7007 | 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