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RNA sequencing of A673 and monoclonal KO cells treated with DMSO or SP-2509

ABSTRACT: RNA sequencing of A673 and monoclonal KO cells treated with DMSO or SP-2509

PROVIDER: PRJNA768848 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16213520_1.fastq.gz	Fastqsanger.gz
	SRR16213520_2.fastq.gz	Fastqsanger.gz
	SRR16213521_1.fastq.gz	Fastqsanger.gz
	SRR16213521_2.fastq.gz	Fastqsanger.gz
	SRR16213522_1.fastq.gz	Fastqsanger.gz

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RNA sequencing of A673 and monoclonal KO cells treated with DMSO or SP-2509

Project description:RNA sequencing data for a Ewing sarcoma cell line, A673 treated with DMSO or the LSD1 inhibitor, SP-2509. Monoclonal cell lines were generated by CRISPR/Cas9 mediated KO of mitochondrial genes MRPL45, UQCRFS1, and CYC1. These cells were treated with DMSO or SP-2509 to determine mitochondrial gene KO derived drug resistance.

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Project description:The transcriptional profile of LSD1 knockdown in A673 Ewing sarcoma cells mirrors that of EWS/FLI knockdown and LSD1 small molecule inhibition (SP-2509)

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Reversible LSD1 Inhibition with HCI-2509 induces the p53 gene expression signature in high-risk neuroblastoma cells

Project description:Lysine-Specific Demethylase 1 (LSD1) over-expression correlates with poorly differentiated neuroblastoma and predicts poor outcome despite multimodal therapy. We have studied the efficacy of reversible and specific LSD1 inhibition with HCI-2509 in neuroblastoma cell lines and particularly the effect of HCI-2509 on the transcriptomic profile in MYCN amplified NGP cells. Cell survival assays show that HCI-2509 is cytotoxic to poorly differentiated neuroblastoma cell lines in low micromole or lower doses. Transcriptional profiling of NGP cells treated with HCI-2509 shows a significant effect on p53, cell cycle, MYCN and hypoxia pathway gene sets. HCI-2509 results in increased histone methyl marks and p53 levels along with cell cycle arrest in the G2/M phase and inhibition of colony formation of NGP cells. Our findings indicate that LSD1 inhibition with HCI-2509 has a multi-target effect in MYCN amplified high-risk neuroblastoma cells.

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