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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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE42388 | GEO | 2013/07/01

SECONDARY ACCESSION(S): PRJNA181265

REPOSITORIES: GEO

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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. 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

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

Project description:Tumor cells at the tumor margin lose epithelial properties and acquire features of mesenchymal cells, a process called epithelial-to-mesenchymal transition (EMT). Recently, features of EMT were shown to be linked to cells with tumor-founding capability, so-called cancer stem cells (CSCs). Inducers of the EMT include several transcription factors, such as Snail (SNAI1) and Slug (SNAI2), as well as the secreted transforming growth factor (TGFß). In the present study, we found that EMT induction in MCF10A cells by stably expressing SNAI1 contributed to drug resistance and acquisition of stem/progenitor-like character as shown by increased cell population for surface marker CD44(+)/CD24(-) and mammosphere forming capacity. Using a microarray approach, we demonstrate that SNAI1 overexpression results in a dramatic change in signaling pathways involved in the regulation of cell death and stem cell maintenance. We showed that NF-κB/MAPK signaling pathways are highly activated in MCF10A-SNAI1 cells by IL1ß stimulation, leading to the robust induction in IL6 and IL8. Furthermore, MCF10A-SNAI1 cells showed enhanced TCF/ß-catenin activity responding to the exogenous Wnt3a treatment. However, EMT-induced stem/progenitor cell activation process is tightly regulated in non-transformed MCF10A cells, as WNT5A and TGFB2 are strongly upregulated in MCF10A-SNAI1 cells antagonizing canonical Wnt pathway. In summary, our data provide new molecular findings how EMT contributes to the enhanced chemoresistance and the acquisition of stem/progenitor-like character by regulating signaling pathways.

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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

Snai1 regulates cell lineage allocation and stem cell maintenance in the mouse intestinal epithelium

Project description:Conditional knockout of Snai1 in the mouse intestinal epithlium results in apoptotic loss of crypt base columnar cells and bias towards differentiation of secretory lineages. In vitro organoid cultures derived from Snail conditional knockout mice also undergo apoptosis when Snai1 is deleted. Snai1 is required for regulation of lineage choice and maintenance of CBC stem cells.

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Snai1 regulates cell lineage allocation and stem cell maintenance in the mouse intestinal epithelium

2015-02-28 | E-GEOD-65005 | biostudies-arrayexpress

SNAI1 induced epithelial to mesenchymal transition miRNA study in time course

Project description:To identify miRNAs participating in SNAI1-orchestrated regulatory pathways, we analysed time-resolved microarray data of SNAI1-induced EMT, obtained during conditional expression of SNAI1 in a “Tet-Off” MCF7-SNAI1 breast carcinoma cell model (Vetter et al, 2009).

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SNAI1 knockdown under VEGF stimulus in HUVECs

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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The SNAI1 and SNAI2 embryonic genes are reactivated in numerous cancer types, including carcinomas

Project description:The SNAI1 and SNAI2 embryonic genes are reactivated in numerous cancer types, including carcinomas. They promote cancer cell dissemination by inducing an epithelial-to-mesenchymal transition (EMT) and by protecting cells from anoikis. We now have demonstrated that the sequentially related SNAI3 gene is aberrantly reactivated in human breast carcinomas. To compare the functional properties of the three SNAIL family members, the transcription factors were ectopically expressed in immortalized mammary epithelial cells. Immortalized human mammary epithelial cells (HMEC-hTERT cells) or MCF10A cells were infected with SNAIL retroviral expression constructs. The gene expression profiles of the resulting cell lines, cultured in standard conditions or after plating them 24h in low-adherent (LA) conditions, were performed.

2013-09-30 | E-GEOD-40690 | biostudies-arrayexpress

SNAI1 overexpression effect on MCF-10A mammary epithelial cell line (mRNA)

Project description:SNAI1 is a key transcription factor in the EMT process, that is considered as the initial step of metastasis. A lot of genes invovled in SNAI1-induced EMT may play important roles in regulating the process of metastasis. We used microarrays to establish the gene expression in SNAI1-induced EMT process.

2016-05-27 | GSE81929 | GEO

SNAI1 overexpression effect on MCF-10A mammary epithelial cell line (miRNA)

Project description:SNAI1 is a key transcription factor in the EMT process, that is considered as the initial step of metastasis. The microRNAs(miRNAs) invovled in SNAI1-induced EMT may play important roles in regulating the process of metastasis. We used microarrays to establish the miRNAs both upregulated and downregulated in SNAI1-induced EMT process.

2016-05-27 | GSE81930 | GEO

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