Generation and characterization of Myc knockin mouse model of osteosarcoma
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ABSTRACT:
PROVIDER: PRJNA967741 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR24455573_1.fastq.gz | Fastqsanger.gz | |||
| SRR24455573_2.fastq.gz | Fastqsanger.gz | |||
| SRR24455574_1.fastq.gz | Fastqsanger.gz | |||
| SRR24455574_2.fastq.gz | Fastqsanger.gz | |||
| SRR24455575_1.fastq.gz | Fastqsanger.gz |
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Project description:To understand the mechanisms that underlie the ability of Myc to alter both the tumor and its surrounding tumor microenvironment (TME) of osteosarcoma, we generated and molecularly characterized an osteoblast-specific Cre-Lox-Stop-Lox;(LSL)-c-MycT58A;p53fl/+ knockin genetically engineered mouse model (GEMM). Phenotypically, the Myc knockin-GEMM had rapid tumor development with a high incidence of metastasis.
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Project description:WWOX promotes osteosarcoma development via upregulation of Myc
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Project description:Osteosarcoma, derived from mesenchymal stem cells or osteoblasts, is the most common malignant bone tumor and the highly metastatic malignant phenotypes often with poor prognosis are related to modulation of TP53- and cell cycle-related pathways. MYC, which regulates the transcription of cell-cycle modulating genes, e.g. CCNE1, is used as a representative prognostic marker. MYCN, a member of MYC oncoprotein family, is highly expressed in a subset of osteosarcoma, however, its roles in osteosarcoma have not been elucidated extensively. Here, we attempted to make an in vitro tumorigenesis model by using hiPSCs derived neural crest cells, which is a precursor cell of mesenchymal stem cells, by MYCN overexpression in the background of heterozygousTP53 hotspot mutation (c.733G>A; p.G245S). MYCN-expressing transformed clones with TP53 mutation were isolated by soft agar colony formation, and injected subcutaneously and into periadrenal adipose tissue of immune-deficient mice, resulted in development of chondroblastic osteosarcoma. MYCN suppression decreased proliferation in MYCN-induced osteosarcoma cells, suggesting that MYCN seems to be one of the targets of osteosarcoma treatment. Further, comprehensive analysis of gene expression and exome sequencing of the MYCN-induced transformed clones indicated molecular context of osteosarcoma-specific feature such as activation of TGF-β signaling and DNA copy number amplification of GLI1. The model of MYCN-expressing chondroblastic osteosarcoma was developed from hiPSC-based neural crest cells, allowing us to provide useful tool for development of new tumor models using hiPSC-derived progenitor cells with gene modification and in vitro transformation.
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Project description:expression analysis from a genetically engineered mouse model of osteosarcoma; determine the expression profile of mouse osteosarcoma Experiment Overall Design: 3 control in vitro differentiated WT primary osteoblasts; 15 primary osteosarcoma; 4 OS cell lines; 4 secondary tumours
2008-10-20 | E-GEOD-9460 | biostudies-arrayexpress
Project description:Osteosarcoma (OS) is an aggressive bone tumor that primarily affects children and adolescents. This malignant tumor is highly aggressive, associated with poor clinical outcomes, and metastasizes mainly to the lungs. Due to its rarity and biological heterogeneity, limited studies of its molecular basis exist, thus hindering the development of effective therapies. WW domain-containing oxidoreductase (WWOX) spans one of the most active and common fragile sites that is frequently altered in human OS. The combined deletion of Wwox and Trp53 using Osterix1-Cre transgenic mice has been shown to accelerate OS development. In this study, we generated a traceable OS mouse model, SKO-Trp53 or DKO-Wwox/Trp53, expressing a tdTomato reporter. By tracking tomato expression at different time points, we detected the early presence of tdTomato-positive cells in the bone marrow (BM) mesenchymal stem cells (MSCs) of non-OS bearing mice, young BM (yBM). We found that DKO yBM cells, but not SKO yBM cells, exhibited tumorigenic traits both in vitro and in vivo. Molecular and cellular characterization of these DKO yBM cells revealed their resemblance to OS tumor cells. Interestingly, one of the observed significant transcriptomic changes in DKO yBM was the upregulation of Myc and its target genes, as compared to SKO yBM cells. Intriguingly, Myc-chromatin immunoprecipitation sequencing (ChIP-Seq) revealed increased enrichment on Myc targets, which were upregulated in DKO yBM cells. Restoration of WWOX in DKO-yBM cells reduced Myc protein levels. As a prototype target, we demonstrated upregulation of MCM7, a known Myc target, in DKO yBM relative to SKO yBM. Inhibition of MCM7 expression using Simvastatin resulted in reduced proliferation and tumor cell growth of DKO yBM cells. Our findings revealed BM-MSCs as a platform to study OS and Myc and its targets as WWOX effectors and early molecular events during osteosarcomagenesis.
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Project description:Osteosarcoma (OS) is an aggressive bone tumor that primarily affects children and adolescents. This malignant tumor is highly aggressive, associated with poor clinical outcomes, and metastasizes mainly to the lungs. Due to its rarity and biological heterogeneity, limited studies of its molecular basis exist, thus hindering the development of effective therapies. WW domain-containing oxidoreductase (WWOX) spans one of the most active and common fragile sites that is frequently altered in human OS. The combined deletion of Wwox and Trp53 using Osterix1-Cre transgenic mice has been shown to accelerate OS development. In this study, we generated a traceable OS mouse model, SKO-Trp53 or DKO-Wwox/Trp53, expressing a tdTomato reporter. By tracking tomato expression at different time points, we detected the early presence of tdTomato-positive cells in the bone marrow (BM) mesenchymal stem cells (MSCs) of non-OS bearing mice, young BM (yBM). We found that DKO yBM cells, but not SKO yBM cells, exhibited tumorigenic traits both in vitro and in vivo. Molecular and cellular characterization of these DKO yBM cells revealed their resemblance to OS tumor cells. Interestingly, one of the observed significant transcriptomic changes in DKO yBM was the upregulation of Myc and its target genes, as compared to SKO yBM cells. Intriguingly, Myc-chromatin immunoprecipitation sequencing (ChIP-Seq) revealed increased enrichment on Myc targets, which were upregulated in DKO yBM cells. Restoration of WWOX in DKO-yBM cells reduced Myc protein levels. As a prototype target, we demonstrated upregulation of MCM7, a known Myc target, in DKO yBM relative to SKO yBM. Inhibition of MCM7 expression using Simvastatin resulted in reduced proliferation and tumor cell growth of DKO yBM cells. Our findings revealed BM-MSCs as a platform to study OS and Myc and its targets as WWOX effectors and early molecular events during osteosarcomagenesis.
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