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Effect of CHD4 and EWS-FLI1 knockdown on gene expression of Ewing sarcoma cells.

ABSTRACT: Effect of CHD4 and EWS-FLI1 knockdown on gene expression of Ewing sarcoma cells.

PROVIDER: PRJNA929293 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23268633_1.fastq.gz	Fastqsanger.gz
	SRR23268633_2.fastq.gz	Fastqsanger.gz
	SRR23268634_1.fastq.gz	Fastqsanger.gz
	SRR23268634_2.fastq.gz	Fastqsanger.gz
	SRR23268635_1.fastq.gz	Fastqsanger.gz

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Effect of CHD4 and EWS-FLI1 knockdown on gene expression of Ewing sarcoma cells.

Project description:We established Ewing sarcoma cells (SKNMC) stably expressing doxycycline-inducible shRNAs targeting the NuRD component CHD4 or the fusion transcription factor EWS-FLI1 to study their influence in gene expression regulation.

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USP1 expression driven by EWS-FLI1 transcription factor stabilizes Survivin and promotes Ewing sarcoma cell survival

Project description:Ewing sarcoma (EWS) is a malignant pediatric bone cancer. Most Ewing sarcomas are driven by EWS-FLI1 oncogenic transcription factor that plays roles in transcriptional regulation, DNA damage response, cell cycle checkpoint control, and alternative splicing. USP1, a deubiquitylase which regulates DNA damage and replication stress responses, is overexpressed at both the mRNA and protein levels in EWS cell lines compared to human mesenchymal stem cells, the EWS cell of origin. The functional significance of high USP1 expression in Ewing sarcoma is not known. Here, we identify USP1 as a transcriptional target of EWS-FLI1 and a key regulator of EWS cell survival. We show that EWS-FLI1 knockdown decreases USP1 mRNA and protein levels. ChIP and ChIP-seq analyses show EWS-FLI1 occupancy on the USP1 promoter. Importantly, USP1 knockdown or inhibition arrests EWS cell growth and induces cell death by apoptosis. We observe destabilization of Survivin (also known as BIRC5 or IAP4) and activation of caspases-3 and -7 following USP1 knockdown or inhibition in the absence of external DNA damage stimuli. Notably, EWS cells display hypersensitivity to combinatorial treatment of doxorubicin or etoposide, EWS standard of care drugs, and USP1 inhibitor compared to single agents alone. Together, our study demonstrates that USP1 is regulated by EWS-FLI1, the USP1-Survivin axis promotes EWS cell survival, and USP1 inhibition sensitizes EWS cells to standard of care chemotherapy.

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Project description:We identified global DNA binding properties of EWS-FLI1 in mouse Ewing sarcoma. GGAA microsatellites were found as binding sites of EWS-FLI1 but with less frequency than that in human Ewing sarcoma, and genomic distribution is not conserved between human and mouse.

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Project description:Identification of genes and pathways that were influenced by knock-down EWS-FLI1 in TC32 Ewing sarcoma cell line.

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