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Gene expression profiles of young and aged mammary epithelial and stromal cell populations from Wild Type and Slug/Snai2-null mice

ABSTRACT: Gene expression profiles of young and aged mammary epithelial and stromal cell populations from Wild Type and Slug/Snai2-null mice

PROVIDER: PRJNA545994 | ENA |

REPOSITORIES: ENA

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Gene expression profiles of young and aged mammary epithelial and stromal cell populations from Wild Type and Slug/Snai2-null mice

Project description:This experiment shows RNA-Seq gene expression profiles of Wild Type and Slug/Snai2-null luminal, basal, and stromal mammary cell populations from young (3 mo) and aged (12 mo) mice.

2019-07-09 | GSE132127 | 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

Hyphthalamic mRNA expression of leptin receptor-expressing cell-specific Slug knockout mice

Project description:Leptin resistance is a driving force for obesity and metabolic syndrome. Slug (Snai2 or Snail2) is an epignetic factor that may play a critical role in the development of leptin resistance in obesity. We conducted a microarray to detect molecular targets of Slug in the hypothalamus.

2022-11-15 | GSE217748 | GEO

Influence of Slug/SNAI2 on global gene expression in CRC cells and tumors

Project description:To establish the role of Slug in CRC, we created a genetic CRC model for Slug expression. As parental cells, we selected HT-29 cells that display a pronounced epithelial phe-notype. HT-29 cells were transfected with Slug, and two stable Slug-expressing clones. (Slug1, Slug2) were isolated. As transfection control, we used HT-29 cells transfected with empty vector (control). To characterize the influence of Slug on gene ex-pression, transcriptome analysis was performed for the four HT-29 cell lines as well as for the corresponding tumor xenografts. Global expression profiling showed that Slug-overexpressing cells and tumors were clustered together while the parental and control cells and tumors formed a separate cluster. Next, a two-step analysis was carried out. First, a subtractive analysis was carried out comparing the gene profiles of Slug-expressing cells and tumors with the corresponding parental/control samples. Genes were considered to be significantly upregulated by Slug if the fold change (FC) was greater than +2 and downregulated if the fold change was less than −2 with p-values (false dis-covery rates) less than 0.01

2022-06-11 | E-MTAB-11812 | biostudies-arrayexpress

Snai2 maintains bone marrow niche cells by repressing osteopontin expression

Project description:Bone marrow (BM) mesenchymal stem and progenitor cells (MSPCs) are a critical constituent of the hematopoietic stem cell (HSC) niche. Previous studies have suggested that the zinc-finger epithelial-mesenchymal transition transcription factor Snai2 (also known as Slug) regulated HSCs autonomously. Here, we show that Snai2 expression in the BM is restricted to the BM stromal compartment where it regulates the HSC niche. Germline or MSPC-selective Snai2 deletion reduces the functional MSPC pool, their mesenchymal lineage output, and impairs HSC niche function during homeostasis and after stress. RNA-sequencing analysis revealed that Spp1 (osteopontin) expression is markedly upregulated in Snai2-deficient MSPCs. Genetic deletion of Spp1 in Snai2-deficient mice, rescues MSPCs’ functions. Thus, SNAI2 is a critical regulator of the transcriptional network maintaining MSPCs by the suppression of osteopontin expression.

2020-04-28 | GSE142705 | GEO

Liver mRNA expression in high fat diet fed mice with hepatic specific Slug knockout

Project description:Liver steatosis is a driving force for nonalcoholic fatty liver disease (NAFLD), alcoholic liver disease, insulin resistance, and type 2 diabetes. Slug (also called Snai2 or Snail2) is a transcriptional regulator that may play a critical role in the regulation of liver function. To prove that, we used microarrays to detail the hepatic Slug regulated gene expression underlying liver steatosis and identified distinct pathways controlled by Slug during this process.

2020-02-18 | GSE145404 | GEO

Influence of Slug/SNAI2 on global gene expression in CRC cells and tumors

Project description:Influence of Slug/SNAI2 on global gene expression in CRC cells and tumors

| PRJEB53433 | ENA

Cell state transitions regulated by Slug are critical for tissue regeneration and tumor initiation [Agilent microarray samples]

Project description:Alterations that perturb differentiation and cell state transitions can lead to defects in development, function and the genesis of cancer. Studying cellular plasticity at high resolution and in real time has proven difficult using existing methods. Here, we use a quantitative approach to gain insights into cell state dynamics of normal mammary epithelial cells (MECs) and validate the model's predictions in vivo. In the absence of Slug/SNAI2, basal mammary progenitor cells transition into a luminal differentiation state, while luminal progenitor cells proliferate and expand; these changes result in abnormal mammary architecture and defects in tissue function. Loss of Slug also disrupts cellular plasticity leading to defects in tissue regeneration and the initiation of cancer. Mechanistically, Slug promotes cellular plasticity by recruiting the chromatin modifier, LSD1 (lysine specific demethylase 1), to promoters of lineage specific genes to represses transcription. Together, these finding demonstrate that Slug is necessary for cellular adaptation during tissue development and regeneration, and that transitioning back into a more primitive stem-like state is a prerequisite for tumor initiation. reference x sample

2014-06-23 | E-GEOD-54713 | biostudies-arrayexpress

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

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