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ChIP-sequencing of Snai1 transcription factor in triple negative breast cancer cell line Hs578T

ABSTRACT: ChIP-sequencing of Snai1 transcription factor in triple negative breast cancer cell line Hs578T

PROVIDER: PRJEB18010 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR1736540.fastq.gz	Fastqsanger.gz
	ERR1736541.fastq.gz	Fastqsanger.gz
	ERR1736538.fastq.gz	Fastqsanger.gz
	ERR1736539.fastq.gz	Fastqsanger.gz

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ChIP-sequencing of Snai1 transcription factor in triple negative breast cancer cell line Hs578T

Project description:This experiment is performed to reveal the novel binding sites of Snai1 transcription factor globally in triple negative breast cancer cell line Hs578T. We also reveal the effect of TGF cytokine on the binding sites of Snai1.

2018-04-25 | E-MTAB-5242 | biostudies-arrayexpress

Ampliseq transcriptomic array of REF seq. genes in Snai1 knock out triple negative breast cancer cells

Project description:Aim of this study is to unveil the global transcriptomic expression levels upon Knockout of Snai1 in triple negative breast cancer cells Hs578T.

2018-04-25 | E-MTAB-5244 | biostudies-arrayexpress

ChIP-sequencing of ZEB1 in triple negative breast cancer cell line Hs578T

Project description:This experiment is performed to reveal the novel binding sites of ZEB1 transcription factor globally in triple negative breast cancer cell line Hs578T. We also reveal the effect of TGF cytokine on the binding sites of ZEB1.

2018-04-25 | E-MTAB-5241 | biostudies-arrayexpress

Role of CCN3 on Hs578T triple negative breast cancer cell line

Project description:Transcriptome sequencing analysis of Hs578T control (CTRL sh) and CCN3 knockdown (CCN3 sh) cell lines. CCN3, also known as nephroblastoma overexpressed (NOV, NOVH), has been associated with cell migration, invasion, angiogenesis, adhesion and proliferation in several cancer types like Ewing’s sarcoma, glioma, prostate cancer, hepatocellular carcinoma, clear cell renal cell carcinoma, chondrosarcoma and melanoma. These results provide information about gene expression affected by CCN3 in triple-negative breast cancer cell lines.

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Project description:To investigate the effect of SNAI1 Knockout on development and growth of triple-negative human breast cancer cells The transcription factor SNAI1 mediates epithelial-mesenchymal transition, fibroblast activation and controls inter-tissue migration. High SNAI1 expression characterizes metastatic triple-negative breast carcinomas, and its knockout by CRISPR/Cas9 uncovered establishment of an epithelio-mesenchymal phenotype accompanied by reduced signaling by the cytokine TGF-β. The SNAI1 knockout cells exhibited plasticity in differentiation, drifting towards the luminal phenotype, gained stemness potential and could differentiate into acinar mammospheres in 3D culture. Loss of SNAI1 derepressed the transcription factor FOXA1, a pioneering factor of mammary luminal progenitors. FOXA1 induced a specific gene program, including the androgen receptor (AR). Inhibiting AR via a specific antagonist regenerated the basal phenotype and blocked acinar differentiation. Thus, loss of SNAI1 in the context of triple-negative breast carcinoma cells promotes an intermediary luminal progenitor phenotype that gains differentiation plasticity, based on the dual transcriptional action of FOXA1 and AR. This function of SNAI1 provides means to separate cell invasiveness from progenitor cell de-differentiation as independent cellular programs.

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Role of CCN3 on Hs578T triple negative breast cancer cell line

Project description:Role of CCN3 on Hs578T triple negative breast cancer cell line

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SMAD2 binding regions in triple negative breast cancer cell line, Hs578T

Project description:SMAD2 binding regions in triple negative breast cancer cell line, Hs578T

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ChIP-sequencing of ZEB1 in triple negative breast cancer cell line Hs578T

Project description:ChIP-sequencing of ZEB1 in triple negative breast cancer cell line Hs578T

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SMAD2 binding regions in triple negative breast cancer cell line, Hs578T

Project description:Inhibitors for cyclin-dependent kinase (CDK) 4 and CDK6 have been established as effective therapeutic options for hormone receptor (HR)-positive, HER2-negative advanced breast cancer. Although the CDK4/6 inhibitors mainly target the cyclin D-CDK4/6-retinoblastoma tumor suppressor protein (RB) axis, little is known about clinical impact of inhibiting phosphorylation of other CDK4/6 target proteins. Here, we have focused on other CDK4/6 targets, SMAD proteins. We showed that a CDK4/6 inhibitor Palbociclib and Activin-SMAD2 signaling cooperatively inhibited cell cycle progression of a luminal-type breast cancer cell line T47D. Mechanistically, Palbociclib enhanced SMAD2 binding to the genome through inhibiting linker phosphorylation of the SMAD2 protein by CDK4/6. Comparison of the SMAD2 ChIP-seq data of T47D with those of a triple-negative breast cancer cell line Hs578T indicated that Palbociclib augments different SMAD2-mediated program defined based on types of cells, and enhances SMAD2 binding to the target regions on the genome without affecting its binding pattern. Collectively, the CDK4/6 inhibitor facilitates the cytostatic effects of Activin-SMAD2, while it also enhances its tumor promoting effects depending on types of breast cancer.

2018-10-23 | GSE117496 | GEO

FOXC1 in triple negative breast cancer [ChIP-seq]

Project description:To investigate FOXC1 chromatin binding, and the effect of FOXC1 CRISPR knockout in triple negative breast cancer cell lines MDA-MB-231, MDA-MB-468, Hs578t, and Bt-549.

2024-06-14 | GSE213840 | GEO

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