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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

SUBMITTER: Soyoung Lim

PROVIDER: E-GEOD-42388 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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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.

2013-07-01 | GSE42388 | GEO

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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Gene expression change after LSD1 siRNA treatment in ER-negative breast cancer cells MDA-MB-231

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2011-07-19 | E-GEOD-30775 | biostudies-arrayexpress

SNAI1-mediated epithelial-mesenchymal transition confers chemoresistance and cellular plasticity by regulating genes involved in cell death and stem cell maintenance.

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