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E-MTAB-5244

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

PROVIDER: E-MTAB-5244 | ExpressionAtlas | 2025-01-23

REPOSITORIES: ExpressionAtlas

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			Action	DRS
	E-MTAB-5244-analysis-methods.tsv	Tabular
	E-MTAB-5244-analytics.tsv	Tabular
	E-MTAB-5244-atlasExperimentSummary.Rdata	Rdata
	E-MTAB-5244-configuration.xml	Xml
	E-MTAB-5244-g2_g1-mvaPlot.png	Other

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E-MTAB-5243

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

2025-01-23 | E-MTAB-5243 | ExpressionAtlas

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

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

| PRJEB18008 | ENA

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

| PRJEB17976 | ENA

E-GEOD-44408

Project description:Transcriptomic survey of lymph node-positive vs. - negative ductal breast cancer

2025-01-24 | E-GEOD-44408 | ExpressionAtlas

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

E-GEOD-27447

Project description:FZD7 Plays a Critical Role in Triple Negative Breast Cancer Proliferation

2025-01-24 | E-GEOD-27447 | ExpressionAtlas

E-GEOD-38959

Project description:Gene expression profiling of triple negative breast cancer, normal ductal cells, and normal tissues

2025-01-24 | E-GEOD-38959 | ExpressionAtlas

SMARCA4 loss-of-function induces cisplatin resistance to activate YAP1-dependent epithelial-to-mesenchymal in triple negative breast cancer

Project description:We report transcriptome profiling (RNA-seq) for SMARA4 knock-out to elucidate the association with cisplatin-resistance and SMARCA4 loss-of-function using triple negative breast cancer cell lines.

2021-11-17 | GSE178532 | GEO

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

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.

2022-10-01 | GSE210870 | GEO

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