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

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

PROVIDER: PRJNA867728 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR20993762_1.fastq.gz	Fastqsanger.gz
	SRR20993762_2.fastq.gz	Fastqsanger.gz
	SRR20993763_1.fastq.gz	Fastqsanger.gz
	SRR20993763_2.fastq.gz	Fastqsanger.gz
	SRR20993764_1.fastq.gz	Fastqsanger.gz

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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.

2022-10-01 | GSE210870 | GEO

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

Project description: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 an epithelio-mesenchymal phenotype accompanied by reduced signaling by the cytokine TGFβ. 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 de-repressed 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.

| S-EPMC9519755 | biostudies-literature

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

Identification of a SNAI1 enhancer RNA that drives cancer cell plasticity

Project description:Enhancer RNAs (eRNAs) are a pivotal class of enhancer-derived non-coding RNAs that drive gene expression. Here we identify the SNAI1 enhancer RNA (SNAI1e; SCREEM2) as a key activator of SNAI1 expression and a potent enforcer of transforming growth factor-β (TGF-β)/SMAD signaling in cancer cells. SNAI1e depletion impairs TGF-β-induced epithelial-mesenchymal transition (EMT), migration, in vivo extravasation, stemness, and chemotherapy resistance in breast cancer cells. SNAI1e functions as an eRNA to cis-regulate SNAI1 enhancer activity by binding to and strengthening the enrichment of the transcriptional co-activator bromodomain-containing protein 4 (BRD4) at the local enhancer. SNAI1e selectively promotes the expression of SNAI1, which encodes the EMT transcription factor SNAI1. Furthermore, we reveal that SNAI1 interacts with and anchors the inhibitory SMAD7 in the nucleus, and thereby prevents TGF-β type I receptor (TβRI) polyubiquitination and proteasomal degradation. Our findings establish SNAI1e as a critical driver of SNAI1 expression and TGF-β-induced cell plasticity.

2025-03-06 | GSE274882 | GEO

Phosphorylation of Plectin by Akt3 Promotes Triple-Negative Breast Cancer Cell Invasive Migration

Project description:Phosphorylation of Plectin by Akt3 Promotes Triple-Negative Breast Cancer Cell Invasive Migration

2025-08-22 | PXD067667 |

SNAI1-mediated epithelial-mesenchymal transition confers chemoresistance and cellular plasticity on MCF10A cells by regulating signaling pathways involved in apoptosis and stem cell maintenance

Project description:Stable expression of SNAI1 in MCF10A cells enhanced resistance to cell death and cellular plasticity by regulating signalling pathways involved in apoptotis and stem cell maintenance. To identify changes on gene expression upon SNAI1-induced epithelial-mesenchymal transition, total RNA was purified from MCF10A cells and MCF10A cells stably expressing SNAI1. Three biololgical replicates were used.

2013-07-01 | E-GEOD-42388 | biostudies-arrayexpress

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

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

| PRJEB18010 | ENA

RAGE/SNAIL signaling drives Epithelial-Mesenchymal plasticity in metastatic Triple-Negative Breast Cancer

Project description:Epithelial-Mesenchymal plasticity plays a fundamental role both in embryogenesis and in tumor cell dissemination during tumor progression. The receptor for advanced glycation end products (RAGE) is a driver of cell plasticity in fibrotic diseases; however, its role and molecular mechanism in triple-negative breast cancer (TNBC) remains unclear. Here, we demonstrate that RAGE signaling maintains the mesenchymal phenotype of aggressive TNBC cells by enforcing the expression of SNAIL. We uncover a crosstalk mechanism between the TGF-β and RAGE pathways that is required for the acquisition of mesenchymal traits in TNBC cells. Consistently, RAGE inhibition elicits epithelial features that block migration and invasion capacities. Since RAGE is a sensor of the tumor microenvironment (TME) and the highly glycolytic rate of tumors induces an acidic TME, we modeled acute acidosis in TNBC cells and showed it promotes enhanced production of RAGE ligands and the activation of RAGE-dependent invasive properties. Furthermore, acute acidosis increases SNAIL levels and tumor cell invasion in a RAGE-dependent manner. Finally, we demonstrate that in vivo inhibition of RAGE reduces metastasis incidence and expands survival, consistent with molecular effects that support the relevance of RAGE signaling in EMT plasticity. These results uncover new molecular insights on the regulation of EMT phenotypes in cancer metastasis and provide rationale for pharmacological intervention of this signaling axis.

2023-12-28 | GSE223229 | GEO

SNAI1-mediated epithelial-mesenchymal transition confers chemoresistance and cellular plasticity on MCF10A cells by regulating signaling pathways involved in apoptosis and stem cell maintenance

2013-07-01 | GSE42388 | GEO