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ABSTRACT: Antiviral Properties of the LSD1 Inhibitor SP-2509

PROVIDER: PRJNA562764 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10033000.fastq.gz	Fastqsanger.gz
	SRR10033001.fastq.gz	Fastqsanger.gz
	SRR10033002.fastq.gz	Fastqsanger.gz
	SRR10032995.fastq.gz	Fastqsanger.gz
	SRR10032996.fastq.gz	Fastqsanger.gz

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N'-(1-phenylethylidene)-benzohydrazide cytotoxicity is LSD1 independent and linked to Fe-S cluster disruption in Ewing sarcoma

Project description:The purpose of the study was to investigate the overlap in cytotoxic and gene regulatory activity between reversible LSD1 inhibitor SP-2509 (HCI-2509) and Compounds 15, 19, and 20 which share structural similariy with SP-2509 but lack LSD1 inhibitory activity. Additionally we compared these compounds to RNAi of EWS::FLI1 (iEF) or Luciferase control (iLuc), as has been done with SP-2509, as well as with OG-L002, an irreversible LSD1 inhibitor with minimal cytotoxic activity.

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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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Therapeutic targeting of KDM1A/LSD1 in Ewing sarcoma engages the ER-stress response II

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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Therapeutic targeting of KDM1A/LSD1 in Ewing sarcoma engages the ER-stress response I

Project description:The purpose of this study was to define biomarkers of sensitivty and mechanisms of resistance to the KDM1A/LSD1 inhibtor SP-2509 (HCI-2509) in Ewing sarcoma cell lines. We report that regardless of drug sensitivity all cell lines engage the UPR and ER-stress response following treatment with SP-2509 resulting in apoptotic cytotoxicity. In addition hypersentsitive cell lines shared a common basal transcriptnomic profile, with hypersensitive cell lines signficantly inducing ETS1 which was not observed in sensitive cell lines.

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Expression data of LUAD cell line PC9 treated with 2 uM HCI-2509 for 48 hours

Project description:The epigenetic regulator LSD1 is overepxpressed in lung adenocarcinoma (LUAD). HCI-2509 a LSD1 inhibitor leads to growth arrest in in vitro tumor models. To identify the underlying molecular mechanims behind LSD1 overexpression, we examined the gene expression patterns using microarray in the LUAD cell line PC9 after HCI-2509 treatment

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Expression data of A549 cells treated with 2 µM of HCI-2509 for 48 h

Project description:Inhibition of LSD1 is a novel option for treatment of lung cancer. Using HCI-2509, a specific inhibitor of LSD1, results in a cell cycle arrest as wel as a shift in global histone 3 lysine 4 and lysine 9 dimethylation pattern. Using microarrays we aim to illucidate the changed transcriptome upon treatement of HCI-2509 in lung adenocarcinoma cell line A549.

2017-08-30 | GSE103256 | GEO

Ewing sarcoma resistance to SP-2509 is not mediated through KDM1A/LSD1 mutation I

Project description:The transcriptional profile of A673 parental and SP-2509 Drug resistant cells treated with DMSO and SP-2509 (2uM 48hrs)

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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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Ewing sarcoma resistance to SP-2509 is not mediated through KDM1A/LSD1 mutation II

Project description:The transcriptional profile of A673 parental, and SP-2509 drug resistant washout cells (4 and 6 months)

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