Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA222890 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Cell state transitions regulated by Slug are critical for tissue regeneration and tumor initiation [Agilent microarray samples]
| PRJNA237521 | ENA
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
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.
2014-06-23 | GSE54713 | GEO
Project description:Temporal expression profiling was utilized to define transcriptional regulatory pathways in vivo in a mouse muscle regeneration model. Potential downstream targets of MyoD were identified by temporal expression, promoter data base mining, and gel shift assays; Slug and calpain 6 were identified as novel MyoD targets. Slug, a member of the snail/slug family of zinc finger transcriptional repressors critical for mesoderm/ectoderm development, was further shown to be a downstream target by using promoter/reporter constructs and demonstration of defective muscle regeneration in Slug null mice.
2007-11-06 | E-GEOD-469 | biostudies-arrayexpress
Project description:Cellular plasticity and transitional cellular states are crucial for tissue regeneration across multiple organs. In the pancreas, oncogenic Kras hijacks this program, acting on tissue-specific enhancers to prevent the resolution of acinar-to-ductal metaplasia (ADM) and lock regeneration into a pro-inflammatory state that progresses to cancer. Enhancer transcription, an early event during cellular state transitions, can generate stable enhancer-associated long noncoding RNAs (lncRNAs) positioned near key transcription factors and chromatin contact boundaries, often enriched for disease-associated variants. While enhancer-associated lncRNAs have been implicated in transcriptional regulation and genome organization, their role in pancreas regeneration and cancer initiation has remained unexplored. In this study, we identified epithelial long noncoding RNAs (lncRNAs) and their target genes in PDAC precursor lesion formation. We demonstrate that LINC00673, expressed from a Sox9-associated super-enhancer during pancreatic development, is reactivated in PDAC. Conditional deletion of LINC00673 in the murine pancreatic epithelium accelerates resolution of ADM and significantly impairs PDAC initiation. Furthermore, we highlight a previously unrecognized role of transcribed super-enhancers in facilitating long-range gene regulation and genome organization during pancreatic cancer initiation. Our study identifies a critical function of LINC00673 in regulating both cell-autonomous and non-cell-autonomous processes during pancreas regeneration and Kras-driven cancer initiation. These findings reveal a novel regulatory layer linking developmental enhancer activity to pancreatic disease progression and highlight new therapeutic opportunities targeting regenerative programs at the earliest stages of neoplastic transformation.
2026-01-16 | GSE316458 | GEO
Project description:Temporal expression profiling was utilized to define transcriptional regulatory pathways in vivo in a mouse muscle regeneration model. Potential downstream targets of MyoD were identified by temporal expression, promoter data base mining, and gel shift assays; Slug and calpain 6 were identified as novel MyoD targets. Slug, a member of the snail/slug family of zinc finger transcriptional repressors critical for mesoderm/ectoderm development, was further shown to be a downstream target by using promoter/reporter constructs and demonstration of defective muscle regeneration in Slug null mice. Keywords: other
2003-07-16 | GSE469 | GEO
Project description:microRNA expression profiling of Stage I Lung Adenocarcinoma and non-tumor adjacent tissues. The Nanostring nCounter Human miRNA Expression Assay Kit version 1.6 (Nanostring, Seattle, WA) was used to obtain microRNA profiles of tumor and adjacent non-tumor tissues excised from Stage I Lung Adenocarcinoma patients. Total cellular RNA was extracted from tumor and matching adjacent non-tumor lung using miRNA Kit (QIAGEN), according to the manufacturer’s instructions, and 100 ng were used for hybridization to Nanostring nCounter Human miRNA Expression Assay Kit version 1.6 (Nanostring, Seattle, WA) following processing protocol recommended by the manufacturer.
2015-04-30 | E-GEOD-63805 | biostudies-arrayexpress
Project description:As a rapid Stem11 scoring platform, a custom NanoString nCounter panel was designed. Alongside the Stem11 genes, the previously published LSC17 genes were included as an established transcriptional prognostic system for AML. For data normalization, seven housekeeping genes were further included from a previous custom NanoString nCounter panel. The full list of the 35 genes in our custom panel is provided in the manuscript.
2026-04-21 | E-MTAB-16782 | biostudies-arrayexpress
Project description:This bulk mRNA data was generated using the Nanostring ncounter platform using an io360 pancancer panel of 900 genes as part of a wider project which included spatial transcriptomic data generated using the Nanostring GeoMx platform. In this study we compared tissue surgical resected from patients with colorectal cancer and liver metastases.
2023-02-02 | GSE224235 | GEO