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

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

PROVIDER: PRJNA907041 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17704159_1.fastq.gz	Fastqsanger.gz
	SRR17704159_2.fastq.gz	Fastqsanger.gz
	SRR17704160_1.fastq.gz	Fastqsanger.gz
	SRR17704160_2.fastq.gz	Fastqsanger.gz
	SRR17704161_1.fastq.gz	Fastqsanger.gz

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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]

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

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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 [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

Sox9 directs divergent epigenomic states in brain tumor subtypes

Project description:Epigenetic dysregulation is a universal feature of cancer that results in altered patterns of gene expression that drive malignancy. Brain tumors exhibit subtype-specific epigenetic alterations, however the molecular mechanisms responsible for these diverse epigenetic states remain unclear. Here we show that the developmental transcription factor Sox9 differentially regulates epigenomic states in high-grade glioma (HGG) and ependymoma (EPN). These contrasting roles for Sox9 correspond with protein interactions with histone deacetylating complexes in HGG, and association with the Rela oncofusion in EPN. Together, our studies demonstrate how epigenomic states are differentially regulated in distinct subtypes of brain tumors, while revealing divergent roles for Sox9 in HGG and EPN tumorigenesis.

2022-07-13 | PXD033863 | Pride

Oncogenic role of SOX9-DHCR24-cholesterol biosynthesis axis in IGH-BCL2 positive diffuse large B-cell lymphomas

Project description:Although oncogenicity of the stem cell regulator SOX9 has been implicated in many solid tumors, its role in lymphomagenesis remains largely unknown. In this study, we showed that SOX9 is overexpressed preferentially in a subset of diffuse large B-cell lymphomas (DLBCL) harboring IGH-BCL2 translocations. SOX9 positivity in DLBCL correlates with advanced stage of disease. Silencing of SOX9 decreased cell proliferation, induced G1/S arrest and increased apoptosis of DLBCL cells, both in vitro and in vivo. Whole transcriptome analysis and CHIP-seq assays identified DHCR24, a terminal enzyme in cholesterol biosynthesis, as a direct target of SOX9, which promotes cholesterol synthesis by increasing DHCR24 expression. Enforced expression of DHCR24 was capable of rescuing the phenotypes associated with SOX9 knockdown in DLBCL cells. In DLBCL cell line xenograft models, SOX9 knockdown resulted in lower DHCR24 level, reduced cholesterol content and decreased tumor load. Pharmacological inhibition of cholesterol synthesis also inhibited DLBCL xenograft tumorigenesis, the reduction of which is more pronounced in DLBCL cell line with higher SOX9 expression, suggesting that it may be addicted to cholesterol. In summary, our study demonstrates that SOX9 can drive lymphomagenesis through DHCR24 and the cholesterol biosynthesis pathway. This SOX9-DHCR24-cholesterol 3 biosynthesis axis may serve as a novel treatment target for DLBCL.

2022-01-12 | GSE179960 | GEO

Oncogenic role of SOX9-DHCR24-cholesterol biosynthesis axis in IGH-BCL2 positive diffuse large B-cell lymphomas [RNA-seq]

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Effect of Misexpression of Sox9 on Gastric Differentiation

Project description:To determine if Sox9 was sufficient to drive mucous differentiation in the gastric epithelium, we bred mice carrying alleles for ROSA26rtTA.IRES.EGFP, TetO-Sox9, and Fgf20Cre.GFP. In these mice, cells expressing Cre will induce rtTA from the ROSA26rtTA.IRES.EGFP allele. To explore transcriptional changes following adult misexpression of Sox9, we isolated RNA from the corpus of Fgf20Cre.GFP/Cre.GFP; ROSA26rtTA.IRES.EGFP/rtTA.IRES.EGFP; TetO-Sox9 pup (misexpression animals) and ROSA26rtTA.IRES.EGFP/rtTA.IRES.EGFP; TetO-Sox9 pup (control) animals and performed RNA-sequencing.

2023-08-30 | GSE230101 | GEO

Vascular endothelial cells drive organ fibrosis by inducing the transcription factor Sox9

Project description:Vascular endothelial cells drive organ fibrosis by inducing the transcription factor Sox9

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