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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.

2022-10-01 | GSE210870 | GEO

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

Project description:Knock-down of LSD1 using siRNA approach induced regulation of several proliferation-associated genes in ER-negative breast cancer cells MDA-MB-231. To identify changes on gene expression caused by treatment with siRNA directed against LSD1 (si) or control siRNA (control) in MDA-MB-231 cells, total RNA was purified from the cells after treatment for 6 days (2 rounds of transfection). Three biological replicates were used.

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.

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.

| S-EPMC3684605 | biostudies-literature

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).

2012-01-13 | GSE35074 | GEO

Expression data from control and Snai1 knockout embryonic stem cells (ESCs)

Project description:Snail1 is a master epithelial-mesenchymal trisition (EMT) factor but its role in ESC maintenance is unknown. We used microarrays to compare the global gene expression between control and Snai1 knockout ESCs. RNA extracted from control and Snai1 knockout ESCs were hybridizated on Affymetrix microarrays.

2013-12-10 | E-GEOD-53107 | biostudies-arrayexpress

Targeting genes of AP-2d in the mouse midbrain

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2011-07-31 | E-GEOD-27296 | biostudies-arrayexpress

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.

2019-03-04 | GSE111386 | GEO

Expression data of control (F/F) and Snai1 knockout (KO) Flk1+/- cells

Project description:Snai1 is a master factor of epithelial to mesenchymal transitioin (EMT), however, its role in embryonic stem cell (ESC) differentiation and lineage commitment remains undefined. We used microarrays to compare the global programme of gene expression between control and Snai1 knockout Flk1+ and Flk1- cells sorted from 4 day EBs. Control and Snai1 knockout ESCs were cultured as embryoid bodies in spotaneous differentiation media, 4 days EBs were dissociated and sorted by anti-Flk1 antibody to separated Flk1+ and Flk1- cells, total RNA were collected for Affymetrix microarrays

2013-12-10 | E-GEOD-53108 | biostudies-arrayexpress

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

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