Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNA-seq of shE4F1 or shCTRL SUM159 triple negative breast cancer cell line treated or not with Gemcitabine

ABSTRACT: RNA-seq of shE4F1 or shCTRL SUM159 triple negative breast cancer cell line treated or not with Gemcitabine

PROVIDER: PRJNA526455 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR8707500.fastq.gz	Fastqsanger.gz
	SRR8707501.fastq.gz	Fastqsanger.gz
	SRR8707502.fastq.gz	Fastqsanger.gz
	SRR8707503.fastq.gz	Fastqsanger.gz
	SRR8707504.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 12

Similar Datasets

RNA-seq of shE4F1 or shCTRL SUM159 triple negative breast cancer cell line treated or not with Gemcitabine

Project description:E4F1 is a ubiquitously expressed zinc-finger protein of the Gli-Kruppel family that was first identified, more than 30 years ago, as a cellular target of the adenoviral oncoprotein E1A13S (Ad type V), required for transcriptional regulation of adenoviral genes. In this study we investigated the impact of direct translational target genes on DNA damage response induced by Gemcitabine. To do so, we performed RNAseq SUM159 triple negative breast cancer cell line. SUM159 was tranfected either with shE4F1 OR shscramble treated or not with Gemcitabine for 24 hours.

2022-03-01 | GSE128099 | GEO

ChIP-seq of E4F1 in SUM159 triple negative breast cancer cell line

Project description:E4F1 is a ubiquitously expressed zinc-finger protein of the Gli-Kruppel family that was first identified, more than 30 years ago, as a cellular target of the adenoviral oncoprotein E1A13S (Ad type V), required for transcriptional regulation of adenoviral genes. In order to decipher E4F1 cellular target genes, we performed chromatin immunoprecipitation of endogenous E4F1 in SUM159 triple negative breast cancer cell line. Both input and immunoprecipitated DNA of two independant experiments were exhaustively sequenced and mapped on the human genome (hg38). Peak detection has been achieved with the HOMER suite algorithms.

2022-03-01 | GSE128104 | GEO

ChIP-seq of E4F1 in SUM159 triple negative breast cancer cell line

Project description:ChIP-seq of E4F1 in SUM159 triple negative breast cancer cell line

| PRJNA526474 | ENA

RNA-seq and ChIP-seq in SUM159 triple negative breast cancer cell line

Project description:RNA-seq and ChIP-seq in SUM159 triple negative breast cancer cell line

| PRJNA526625 | ENA

ChIP-seq analysis of HN1L protein in SUM159 triple-negative breast cancer cells

Project description:ChIP-seq analysis of HN1L protein in SUM159 triple-negative breast cancer cells

| PRJNA415189 | ENA

Gene expression profiling of transmitochondrial cybrids (triple negative breast cancer cells in SUM159 background)

Project description:We used a transmitochondrial cybrid (cybrids)-based discovery approach to identify mitochondria-regulated cancer pathways in TN BCa. Cybrids were generated under a moderately metastatic TN BCa cell line SUM159 as the common nuclear background with mitochondria from benign breast epithelium (A1N4) and moderately metastatic (SUM159) TN BCa cells. In vitro and in vivo studies suggested that even under the common moderately cancerous nuclear background, mitochondria from benign cells inhibit and metastatic cell induce cancer properties of a moderately aggressive TN BCa cell. Gene expression studies identified c-Src onco-pathway as one of the major cancer pathways altered according to the mitochondria status of the cybrids. SUM159 Ï0 cells were used as nuclear donor and A1N4 and SUM 159 cells were used as mitochondrial donor cells. The two groups were profiled for gene expression using microarrays. two group comparison (159/SUM159 vs A1/SUM159)

2016-04-14 | E-GEOD-72319 | biostudies-arrayexpress

Expression data from TGFBR3 controls and TGFBR3 knockdown of SUM159 3D cultures

Project description:The objective of this experiment was to determine global gene expression change in triple negative cell line upon knockdown of TGFBR3. Genotype specific differences in expression profiles have been evaluated using human HuGene1.0-ST affymetrix array. RNA was extracted from SUM159 controls and SUM159 TGFBR3KD cells cultured in 3-dimensional in vitro system.

2014-02-06 | GSE54756 | GEO

Response of triple negative breast cancer to BAZ2A/B inhibition and BET bromodomain inhibition alone and in combination (RNAseq)

Project description:Three triple negative breast cancer cell lines (MDAMB231, SUM159, and HCC1806) were treated with small molecule inhibitors (JQ1, BET bromodomain inhibitor; GSK2801, BAZ2A/B bromodomain inhibitor) alone and in combination for 72 hours

2019-07-09 | GSE116907 | GEO

Effect of targeting NOS2 on gene expression of triple-negative breast cancer (metaplastic) SUM159 cell lines

Project description:To investigate the role of iNOS in tumor cell morphology and gene expression, we utilized CRISPR-Cas9 gene editing (NOS2 Double Nickase Plasmid, Santa Cruz) to knockout NOS2 in SUM159 cells. After puromycin selection, resistant clones were selected by immunoblotting for iNOS expression and nitrite/nitrate colorimetric assay. We then performed gene expression profiling analysis using data obtained from RNA-seq of parental SUM159 cells compared to NOS2KO SUM159 cells.

2024-05-28 | GSE234512 | GEO

Transcriptome profiling of SUM159 and derivatives with different metastasis capability

Project description:Triple negative breast cancer cell line SUM159 labeled with triple reporter (TR, TK-GFP-fLUC) injected into Nude mice via mammary fat pad and tail vein injection. Tumor progression is monitored by in vivo bioluminescent imaging. Tumors from mammary and lung were isolated and cultured. These derivatives cells are further tested for their capability to develop mammary primary tumor and metastasis in lung and bone in mice. The total RNA samples are extracted from the panel of SUM159 and derivatives and the transcriptome profiles are determined by microarray. The correlation of transcriptome of the cells to metastasis capability indicated candidate genes and regulatory pathways of metastasis of TNBC.

2021-01-13 | GSE151198 | 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