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Targeted degradation of BRD9 reverses oncogenic gene expression in synovial sarcoma [ChIP-seq]

ABSTRACT: We used a CRISPR-based screening approach to identify functional vulnerabilities in pediatric sarcoma cell types, identifying BRD9 as an important dependency in synovial sarcoma cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE113228 | GEO | 2018/11/01

REPOSITORIES: GEO

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Targeted degradation of BRD9 reverses oncogenic gene expression in synovial sarcoma [RNA-seq]

Project description:We used a CRISPR-based screening approach to identify functional vulnerabilities in pediatric sarcoma cell types, identifying BRD9 as an important dependency in synovial sarcoma cells.

2018-11-01 | GSE113227 | GEO

Targeted degradation of BRD9 reverses oncogenic gene expression in synovial sarcoma

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ATAC-seq of synovial sarcoma cell lines treated with the BRD9 PROTAC degrader WA-68

Project description:Synovial sarcoma (SyS) is driven by the SS18::SSX fusion oncoprotein, which incorporates into GBAF chromatin remodeling complexes and creates a dependency on BRD9. To investigate the effects of BRD9 loss, we performed ChIP-seq, ATAC-seq, and RNA-seq in SyS models following BRD9 degradation. ChIP-seq shows reduced GBAF occupancy at target loci, while ATAC-seq reveals maintained or increased chromatin accessibility. RNA-seq demonstrates sustained or elevated expression of target genes. These results indicate that BRD9 is not required for GBAF assembly but instead restrains its remodeling activity, providing a mechanistic explanation for the limited efficacy of BRD9-targeted therapies in SyS.

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Project description:Targeted degradation of BRD9 reverses oncogenic gene expression in synovial sarcoma [RNA-seq]

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Targeted degradation of BRD9 reverses oncogenic gene expression in synovial sarcoma [ChIP-seq]

Project description:Targeted degradation of BRD9 reverses oncogenic gene expression in synovial sarcoma [ChIP-seq]

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Targeted degradation of BRD9 reverses oncogenic gene expression in synovial sarcoma.

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BRD9 degraders CAN-25-5405-ETR1

Project description:BRD9 degraders unleash GBAFCHromatin Remodeling Activity in Synovial Sarcoma

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Epigenetic regulation of p53 represents a targetable dependency in synovial sarcoma

Project description:Synovial sarcoma is a deadly malignancy of soft-tissue with a predilection for adolescents and young adults that consistently associates with a t(X;18) chromosomal translocation and expression of the resultant fusion oncoprotein SS18::SSX. Here, the dependency on MDM2 that has been observed in multiple synovial sarcoma cell lines is presented. Very few synovial sarcomas in humans demonstrate TP53 mutation or loss, CDKN2A loss, or MDM2 gains, each common among other sarcoma types. Silencing of homologous Trp53 in a mouse model of SS18::SSX-expression-induced sarcomagenesis leads to a slightly reduced latency to tumorigenesis, but no increase in de-differentiated phenotypes, or nuclear pleiomorphism. Transcriptome analysis revealed minimal change in p53 target gene expression, suggesting that expression of the fusion alone was sufficient to impact these. Treatment of mice with the MDM2-p53-intereaction inhibitor, HDM201, was modestly successful at slowing tumor growth, alone. Combined treatment with HDM201 and the HDAC inhibitor panobinostat, known to be capable of derepressing Cdkn2a expression, synergized to curtail synovial sarcoma development.

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