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CFos-Sox9 Axis Reprograms Bone Marrow-derived Mesenchymal Stem Cells into Chondroblastic Osteosarcoma

ABSTRACT: cFos-Sox9 Axis Reprograms Bone Marrow-derived Mesenchymal Stem Cells into Chondroblastic Osteosarcoma

PROVIDER: PRJNA349798 | ENA |

REPOSITORIES: ENA

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cFos-Sox9 Axis Reprograms Bone Marrow-derived Mesenchymal Stem Cells into Chondroblastic Osteosarcoma [RNA-seq]

Project description:The goal is to profile cFos binding sites in an p53 knockout mouse bone marrow-derived stem cells (mBMSCs).

2017-08-11 | GSE89014 | GEO

cFos-Sox9 Axis Reprograms Bone Marrow-derived Mesenchymal Stem Cells into Chondroblastic Osteosarcoma [ChIP-seq]

Project description:The goal is to profile cFos binding sites in an p53 knockout mouse bone marrow-derived stem cells (mBMSCs).

2017-08-11 | GSE88986 | GEO

cFOS-SOX9 Axis Reprograms Bone Marrow-Derived Mesenchymal Stem Cells into Chondroblastic Osteosarcoma.

Project description:Bone marrow-derived mesenchymal stem cells (BMSCs) are proposed as the cells of origin of several subtypes of osteosarcoma (OS). However, signals that direct BMSCs to form different subtypes of OS are unclear. Here we show that the default tumor type from spontaneously transformed p53 knockout (p53_KO) BMSCs is osteoblastic OS. The development of this default tumor type caused by p53 loss can be overridden by various oncogenic signals: RAS reprograms p53_KO BMSCs into undifferentiated sarcoma, AKT enhances osteoblastic OS, while cFOS promotes chondroblastic OS formation. We focus on studying the mechanism of cFOS-induced chondroblastic OS formation. Integrated genome-wide studies reveal a regulatory mechanism whereby cFOS binds to the promoter of a key chondroblastic transcription factor, Sox9, and induces its transcription in BMSCs. Importantly, SOX9 mediates cFOS-induced cartilage formation in chondroblastic OS. In summary, oncogenes determine tumor types derived from BMSCs, and the cFOS-SOX9 axis is critical for chondroblastic OS formation.

| S-EPMC5470112 | biostudies-literature

Mus musculus

Project description:cFos-Sox9 Axis Reprograms Bone Marrow-derived Mesenchymal Stem Cells into Chondroblastic Osteosarcoma [ChIP-seq]

| PRJNA349461 | ENA

Mus musculus

Project description:cFos-Sox9 Axis Reprograms Bone Marrow-derived Mesenchymal Stem Cells into Chondroblastic Osteosarcoma [RNA-seq]

| PRJNA349803 | ENA

cFos-Sox9 Axis Reprograms Bone Marrow-derived Mesenchymal Stem Cells into Chondroblastic Osteosarcoma

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

2017-08-11 | GSE89015 | GEO

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]

2022-01-12 | GSE180051 | GEO

Dynamics and transcriptomic driver landscape of metastatic osteosarcoma

Project description:We report MAPK7-MMP9 signalling axis in metastatic osteosarcoma

2020-07-27 | GSE140131 | GEO

The conserved sex regulator/pioneer factor DMRT1 recruits SOX9 in sexual cell fate reprogramming

Project description:Mammalian sexual development commences when fetal bipotential progenitor cells adopt male Sertoli (in XY) or female granulosa (in XX) gonadal cell fates. Differentiation of these cells involves extensive divergence in chromatin state and gene expression, reflecting distinct roles in sexual differentiation and gametogenesis. Surprisingly, differentiated gonadal cell fates require active maintenance through postnatal life to prevent sexual transdifferentiation and female cell fate can be reprogrammed by ectopic expression of the sex regulator DMRT1. Here we examine how DMRT1 reprograms granulosa cells to Sertoli-like cells in vivo and in culture. We define postnatal granulosa- and Sertoli-biased gene expression programs and identify cell type-biased three-dimensional chromatin contacts and differentially accessible chromatin regions (DARs) associated with differentially expressed genes. Using a conditional transgene we find DMRT1 only partially reprograms the ovarian transcriptome in the absence of SOX9 and its paralog SOX8, indicating that these factors functionally cooperate with DMRT1. ATAC-seq and ChIP-seq show that DMRT1 induces formation of many DARs that it binds with SOX9, and DMRT1 is required for binding of SOX9 at most of these sites. We suggest that DMRT1 can act as a pioneer factor to open chromatin and allow binding of SOX9, which then cooperates with DMRT1 to reprogram sexual cell fate.

2021-05-20 | GSE154484 | GEO

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