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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE40690 | GEO | 2013/09/30

SECONDARY ACCESSION(S): PRJNA174625

REPOSITORIES: GEO

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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

Identification of differentially expressed lncRNAs and coding mRNAs in SNAI1/2 overexpression cell line

Project description:The oncogene SNAI2 is known to be a master transcription factor that regulates a broad range of cellular processes, including epithelial-mesenchymal transition (EMT). As a transcription factor, there is no doubt that SNAI1/2 could directly regulate the expression of thousands of genes, including lncRNAs. In this study, we took SNAI1/2 as a breakthrough point to screen and identify lncRNAs regulated by SNAI2 in GC. Our data showed that overexpression of SNAI2 caused a 1.5-fold change in the expression of about 654 lncRNAs (|Log2FC| >0.5), and a 2-fold change in the expression of about 123 lncRNAs (|Log2FC| >1).

2021-10-01 | GSE161551 | GEO

Homo sapiens

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

| PRJNA174625 | ENA

PARP1-SNAI2 Transcription Axis Drives Resistance to PARP Inhibitor, Talazoparib

Project description:The synthetic lethal association between BRCA deficiency and poly (ADP-ribose) polymerase (PARP) inhibition supports PARP inhibitor (PARPi) clinical efficacy in BRCA-mutated tumors. PARPis also demonstrate activity in non-BRCA mutated tumors presumably through induction of PARP1-DNA trapping. Despite pronounced clinical response, therapeutic resistance to PARPis inevitably develops. An abundance of knowledge has been built around resistance mechanisms in BRCA-mutated tumors, however, parallel understanding in non-BRCA mutated settings remains insufficient. In this study, we find a strong correlation between the epithelial-mesenchymal transition (EMT) signature and resistance to a clinical PARPi, Talazoparib, in non-BRCA mutated tumor cells. Genetic profiling demonstrates that SNAI2, a master EMT transcription factor, is transcriptionally induced by Talazoparib treatment or PARP1 depletion and this induction is partially responsible for the emerging resistance. Mechanistically, we find that the PARP1 protein directly binds to SNAI2 gene promoter and suppresses its transcription. Talazoparib treatment or PARP1 depletion lifts PARP1-mediated suppression and increases chromatin accessibility around SNAI2 promoters, thus driving SNAI2 transcription and drug resistance. We also find that depletion of the chromatin remodeler CHD1L suppresses SNAI2 expression and reverts acquired resistance to Talazoparib. The PARP1/CHD1L/SNAI2 transcription axis might be therapeutically targeted to re-sensitize Talazoparib in non-BRCA mutated tumors.

2022-07-08 | PXD033530 | Pride

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

RNA-seq data of si-Snai1, si-Snai2, si-Snai1/2 and si-Scrambled treated mouse primary myoblasts

Project description:In skeletal myogenesis, the transcription factor MyoD, activates distinct transcriptional programs in progenitors compared to terminally differentiated cells. Using ChIP-seq and gene expression analyses, we show that in primary myoblasts, Snai1/2-HDAC1/2 repressive complex bind and exclude MyoD from its targets. Notably, Snail binds E-box motifs that are G/C-rich in their central dinucleotides, and such sites are almost exclusively associated with genes expressed during differentiation. By contrast, Snai1/2 does not bind the A/T-rich E-boxes associated with MyoD targets in myoblasts. Thus, Snai1/2-HDAC1/2 prevents MyoD occupancy on differentiation-specific regulatory elements and the change from Snail1/2- to MyoD-binding often results in enhancer switching during differentiation. Furthermore, we show that a regulatory network involving Myogenic Regulatory Factors (MRFs), Snail/2, miR-30a and miR-206 acts as a molecular switch that controls entry into myogenic differentiation. Together, these results reveal a regulatory paradigm that directs distinct gene expression programs in progenitors versus terminally differentiated cells.

2012-07-05 | GSE38236 | GEO

RNA-seq data of si-Snai1, si-Snai2, si-Snai1/2 and si-Scrambled treated mouse primary myoblasts

2012-07-04 | E-GEOD-38236 | biostudies-arrayexpress

Snai2 influences breast cancer evolution in a non-cell autonomous manner

Project description:SNAI2 is a transcription factor involved in multiple processes in both physiology and pathology, including apoptosis, epithelial-mesenchymal transition and tumorigenesis. The effects of SNAI2 on the epithelial compartment have been interpreted as an effect of its expression and action in that compartment. In this work, we demonstrated that the absence of Snai2 in other compartments has repercussions in different aspects of the behavior of the epithelial cells of luminal breast tumors, developed by MMTV-ErbB2/Neu transgenic mice that do not express SNAI2 in the epithelial component. The absent of SNAI2 in the stroma of these tumors is accompanied by different characteristics at histopathological and molecular levels than those having functional SNAI2. These results indicate that the expression of SNAI2 in the tumor niche contributes to the luminal tumor development and behavior.

2018-03-20 | GSE112052 | GEO

Genome Wide Expression of Mammary Epithelial Populations in Slug (SNAI2) WT vs Slug Null Mice

Project description:This experiment shows differential expression of genes in the luminal, basal and stromal subpopulations from SNAI2+/+ and SNAI2 LacZ/LacZ mammary epithelial cells. Luminal, basal and stromal populations were sorted from SNAI2+/+ and SNAI2 LacZ/LacZ mammary epithelial cells based on expression of CD49f and Epcam.

2014-03-08 | E-GEOD-55620 | biostudies-arrayexpress

Genome Wide Expression of Mammary Epithelial Populations in Slug (SNAI2) WT vs Slug Null Mice

Project description:This experiment shows differential expression of genes in the luminal, basal and stromal subpopulations from SNAI2+/+ and SNAI2 LacZ/LacZ mammary epithelial cells.

2014-03-08 | GSE55620 | GEO

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