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

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

PROVIDER: PRJEB18008 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR1736470.fastq.gz	Fastqsanger.gz
	ERR1736465.fastq.gz	Fastqsanger.gz
	ERR1736466.fastq.gz	Fastqsanger.gz
	ERR1736467.fastq.gz	Fastqsanger.gz
	ERR1736468.fastq.gz	Fastqsanger.gz

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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.

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Ampliseq transcriptomic array of REF seq. genes in ZEB1 knock out triple negative breast cancer cells

Project description:Ampliseq transcriptomic array of REF seq. genes in ZEB1 knock out triple negative breast cancer cells

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Ampliseq transcriptomic array of REF seq. genes in ZEB1 knock out triple negative breast cancer cells

Project description:Aim of this study is to unveil the global transcriptomic expression levels upon Knockout of ZEB1 in triple negative breast cancer cells Hs578T.

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Loss of SNAI1 induces cellular plasticity in invasive triple-negative breast cancer cells

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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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.

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AmpliSeq transcriptome profiling of human adipose tissue senescent progenitor cells

Project description:Transcriptomic profile of human adipose tissue progenitor cells was performed as follows. For AmpliSeq transcriptome sequencing library construction, AmpliSeq™ Library PLUS, AmpliSeq Transcriptome Human Gene Expression Panel and AmpliSeq CD indexes SetA kits were purchased from Illumina and sequencing libraries were constructed as described in AmpliSeq for Illumina Transcriptome Human Gene Expression Panel reference guide (Illumina). Equimolar concentrations of libraries were pooled at 4 nM and denatured and diluted as described in Denature and Dilute Libraries Guide (Illumina) and adjusted to final concentration of 1.4 pM. Resulting library was sequenced on NextSeq 500 using NextSeq 500/550 High Output v2 kit with 2 X 151 bp cycle. Generated raw files were converted to FASTQ files and used for data analysis. AmpliSeq transcriptome FASTQ files were analyzed on Array studio V10.0 (Omicsoft, Qiagen). Following raw read QC, first and last 10 bases were trimmed and mapped to reference genome Human.B38. The read count data was generated using GeneModel RefGene20170606. Resulting data was normalized by DESeq package, transformed to log2 value and used for ANOVA analyses.

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Project description:The goal of this study was to reveal SNAI1 function in angiogenesis. SNAI1 is up-regulated by VEGF stimulus. Using RNASeq method (single-ended 150-bp sequencing on Illumina Hi-seq 3000 instrument), we measured the transcriptional difference between siSNAI1 or NC-transfected HUVECs.

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