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

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

PROVIDER: PRJNA526625 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8707500.fastq.gz	Fastqsanger.gz
	SRR8707600.fastq.gz	Fastqsanger.gz
	SRR8707501.fastq.gz	Fastqsanger.gz
	SRR8707601.fastq.gz	Fastqsanger.gz
	SRR8707502.fastq.gz	Fastqsanger.gz

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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

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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

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

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

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

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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.

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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)

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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

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