Phase Separation of ARID1A Chromatin Remodeling Factor Promotes Oncogenic Potential of Ewing’s Sarcoma
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ABSTRACT:
PROVIDER: PRJNA980606 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR24837354_1.fastq.gz | Fastqsanger.gz | |||
| SRR24837354_2.fastq.gz | Fastqsanger.gz | |||
| SRR24837355_1.fastq.gz | Fastqsanger.gz | |||
| SRR24837355_2.fastq.gz | Fastqsanger.gz | |||
| SRR24837356_1.fastq.gz | Fastqsanger.gz |
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Project description:We charaterized the effect of ARID1A phase separation on transcriptome/epigenome/3D chromatin structure in Ewing's Sarcoma cancer cell line
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Project description:Ewing’s sarcoma is highly malignant bone tumor that involves childhood and adolescent, and its nature has not been well understood. To clarify its cellular origin and the mechanisms of tumorigenesis, we used ex vivo approach to create a murine model for Ewing’s sarcoma. The osteochondrogenic progenitors derived from the facial zone (FZ) of murine long bones at late gestation were purified by microdissection, introduced with EWS-FLI1 or EWS-ERG retroviruses and transplanted into nude mice. Ewing’s sarcoma-like small round cell sarcoma developed at 100% penetrance, whereas tumor induction was less effective when growth place (GP)-derived cells were used. The different response of gene expression to EWS-FLI1 between FZ and GP cells suggests importance of the specific cellular context for EWS-FLI1 to induce Ewing’s sarcoma. The Wnt/β-catenin pathway was involved in close relationship to the cellular context, with Dkk2 and Wipf1 as important downstream modulators. Furthermore, gene expression profiling revealed similarity between our models and human Ewing’s sarcoma. These results indicate that Ewing’s sarcoma originates from the embryonic osteochondrogenic progenitor.
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