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A SOX9-B7x axis safeguards dedifferentiated tumor cells from immune surveillance to drive breast cancer progression [RNA-seq and ChIP-seq]

ABSTRACT: A SOX9-B7x axis safeguards dedifferentiated tumor cells from immune surveillance to drive breast cancer progression [RNA-seq and ChIP-seq]

PROVIDER: PRJNA799601 | ENA |

REPOSITORIES: ENA

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A SOX9-B7x axis safeguards dedifferentiated tumor cells from immune surveillance to drive breast cancer progression [RNA-seq and ChIP-seq]

Project description:The transcription factor SOX9 can act as a pioneering factor in driving lineage dedifferentiation and tumor progression for breast cancer. To investigate downstream pathways mediating SOX9 function and identify the direct gene targets of SOX9, we performed RNA-seq and SOX9 ChIP-seq on human breast cancer cell line MCF7ras ctrl and SOX9-overexpressing (SOX9OE) cells.

2023-10-16 | GSE194201 | GEO

A SOX9-B7x axis safeguards dedifferentiated tumor cells from immune surveillance to drive breast cancer progression

Project description:A SOX9-B7x axis safeguards dedifferentiated tumor cells from immune surveillance to drive breast cancer progression

| PRJNA907041 | ENA

A SOX9-B7x axis safeguards dedifferentiated tumor cells from immune surveillance to drive breast cancer progression [10X scRNA-seq]

Project description:A SOX9-B7x axis safeguards dedifferentiated tumor cells from immune surveillance to drive breast cancer progression [10X scRNA-seq]

| PRJNA907045 | ENA

A SOX9-B7x axis safeguards dedifferentiated tumor cells from immune surveillance to drive breast cancer progression [10X scRNA-seq]

Project description:The transcription factor SOX9 can act as a pioneering factor in driving lineage dedifferentiation and tumor progression for breast cancer. To unbiasedly understand how committed luminal stem progenitor cells dedifferentiate into embryonic multipotent progenitor-like cells, we performed scRNA-seq in luminal cells FACS sorted from WT control mice and Sox9-GFP;C3-TAg mice at the age of 3.5 months when C3-TAg mice have developed extensive hyperplastic lesions but not yet malignant tumors.

2023-10-16 | GSE219109 | GEO

A SOX9-B7x axis safeguards dedifferentiated tumor cells from immune surveillance to drive breast cancer progression

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-10-16 | GSE219110 | GEO

The transcription factors SOX9 and SOX5/SOX6 cooperate genome-wide through super-enhancers to drive chondrogenesis (ChIP-Seq)

Project description:SOX9 is a transcriptional activator required for chondrogenesis, and SOX5 and SOX6 are closely related DNA-binding proteins that critically enhance its function. We used RNA-seq to charatierize a rat chondrosarcoma (RCS) cells as a faithful model for proliferating/early prehypertrophic growth plate chondrocytes and ChIP-seq to gain novel insights into the full spectrum of the target genes and modes of action of this chondrogenic trio. ChIP-seq for SOX9, SOX6 and histone modifications were carried out using RCS cells

2015-06-23 | E-GEOD-70143 | biostudies-arrayexpress

The transcription factors SOX9 and SOX5/SOX6 cooperate genome-wide through super-enhancers to drive chondrogenesis (RNA-Seq)

Project description:SOX9 is a transcriptional activator required for chondrogenesis, and SOX5 and SOX6 are closely related DNA-binding proteins that critically enhance its function. We used RNA-seq to charatierize a rat chondrosarcoma (RCS) cells as a faithful model for proliferating/early prehypertrophic growth plate chondrocytes and ChIP-seq to gain novel insights into the full spectrum of the target genes and modes of action of this chondrogenic trio. RNAs were isolated from three bioogical replicatse of rat chondrosarcoma (RCS) cells and rib samples for RNA-seq experiments.

2015-06-23 | E-GEOD-70142 | biostudies-arrayexpress

Endothelial cells drive organ fibrosis and dysfunction by inducing the transcription factor SOX9 (ATAC-Seq)

Project description:Fibrosis is a hallmark of chronic disease. Although fibroblasts are known to be involved, it is unclear to what extent endothelial cells might contribute. We detected increased expression of the transcription factor Sox9 in endothelial cells of fibrotic mouse organs in models of systolic heart failure by pressure overload, diastolic heart failure by high-fat diet and L-Name administration, pulmonary fibrosis after bleomycin treatment, and liver fibrosis as consequence of CDAA diet. We also observed endothelial SOX9 upregulation in human heart tissue in patients with heart failure. To test whether this SOX9 induction was sufficient to cause disease, we generated mice with endothelial cell-specific overexpression of Sox9, which indeed triggered extensive fibrosis in multiple organs and promoted signs of heart failure. Endothelial Sox9 deletion, in turn, prevented fibrosis and organ dysfunction in pre-clinical surgical and pharmacological mouse models of heart failure as well as of lung, and liver injury. Bulk and single cell RNA sequencing of endothelial cells across multiple vascular beds revealed that SOX9 induced extracellular matrix, growth factor, and inflammatory genes leading to matrix deposition by endothelial cells. Moreover, in part through triggering an increased expression of the secreted growth factor Ccn2 as direct SOX9 target, endothelial cells activated neighboring fibroblasts to migrate and deposit matrix in response to SOX9. Endothelial Sox9 deletion reversed these changes, suggesting a role for endothelial SOX9 as fibrosis-promoting transcription factor across organs in response to disease stimuli. Therefore, endothelial cells could be a promising target to counteract fibrotic heart, liver and lung disease

2023-12-29 | GSE252081 | GEO

Sox9 determines translational capacity during early chondrogenic differentiation of ATDC5 cells by regulating expression of ribosome biogenesis factors and ribosomal proteins

Project description:Introduction: In addition to the well-known cartilage extracellular matrix-related expression of Sox9, we demonstrated that chondrogenic differentiation of progenitor cells is driven by a sharply defined bi-phasic expression of Sox9: an immediate early and a late (extracellular matrix associated) phase expression. In this study we aimed to determine what biological processes are driven by Sox9 during this early phase of chondrogenic differentiation. Materials: Sox9 expression in ATDC5 cells was knocked-down by siRNA transfection at the day before chondrogenic differentiation or at day 6 of differentiation. Samples were harvested at 2 hours, and 7 days of differentiation. The transcriptomes (RNA-seq approach) and proteomes (Label-free proteomics approach) were compared using pathway and network analyses. Total protein translational capacity was evaluated with the SuNSET assay, active ribosomes with polysome profiling and ribosome modus with bicistronic reporter assays. Results: Early Sox9 knockdown severely inhibited chondrogenic differentiation weeks later. Sox9 expression during the immediate early phase of ATDC5 chondrogenic differentiation regulated the expression of ribosome biogenesis factors and ribosomal protein subunits. This was accompanied by decreased translational capacity following Sox9 knockdown, and this correlated to lower amounts of active mono- and polysomes. Moreover, cap- versus IRES-mediated translation was altered by Sox9 knockdown. Sox9 overexpression was able to induce reciprocal effects to the Sox9 knockdown. Conclusion: Here we identified an essential new function for Sox9 during early chondrogenic differentiation. A role for Sox9 in regulation of ribosome amount, activity and/or composition may be crucial in preparation for the demanding proliferative phase and subsequent cartilage extracellular matrix-production of chondroprogenitors in the growth plate in vivo.

2021-06-18 | PXD024715 | Pride

RNA-seq of purified human pancreatic dedifferentiated acinar cells and duct cells

Project description:Pancreatic acinar cells can dedifferentiate upon tissue injury and acquire ductal characteristics. This acquisition of duct cell features is critical in tumor development. Nevertheless, duct cells themselves are less prone for development of PDAC (pancreatic ductal adenocarcinoma) than dedifferentiated acini. We aimed to clarify which genes are unique for dedifferentiated acini. Mixed exocrine preparations of acinar and duct cells were obtained from human pancreatic donor organs and cultured to induce dedifferentiation. We lineage-labeled and FACS-purified these human dedifferentiated acinar cells and compared them to duct cells from the same donor (n=5).

2021-06-17 | E-MTAB-9386 | biostudies-arrayexpress

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