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RNA-Seq analysis of HL-60 AML cells resistant to daunorubicin or cytarabine

ABSTRACT: RNA-Seq analysis of HL-60 AML cells resistant to daunorubicin or cytarabine

PROVIDER: PRJNA794751 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17446833.fastq.gz	Fastqsanger.gz
	SRR17446834.fastq.gz	Fastqsanger.gz
	SRR17446835.fastq.gz	Fastqsanger.gz
	SRR17446836.fastq.gz	Fastqsanger.gz
	SRR17446837.fastq.gz	Fastqsanger.gz

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RNA-Seq analysis of HL-60 AML cells resistant to daunorubicin or cytarabine

Project description:The Acute Myeloid Leukemia cell line HL-60 was rendered resistant to daunorubicin (DNR) or cytarabine (Ara-C) by continuous exposure to the drug up to concentrations of 30nM for DNR and 100nM for Ara-C. Transcriptomic analysis were then performed by RNA-Seq to compare the cell lines

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Genes rapidly regulated by Ara-C and DNR treatment of HL-60 AML cells and role of NADPH-oxidase derived ROS in DNR-induced gene expression

Project description:Daunorubicin (DNR) and Cytarabin (Ara-C) are the main chemotherapeutic drugs used for Acute Myeloid Leukemias (AML) treatment. However, their mode of action is not well understood. To decipher if these drug would induce rapid transcriptional reprogramming, we treated HL-60 AML cell line with DNR or Ara-C for 3 hours and carried out a transcriptomic analyses. In addition, we had shown that Reactive Oxigen Species (ROS) produced by NADPH oxidases (NOX) are involved in DNR-induced gene expression. We therefore also performed a transcriptomic analyses in HL-60 cells treated with DNR and VAS2870, an NADPH oxidase inhibitor. HL-60 cells were treated or not for 3 hours with 2 ÂµM Ara-C, 1 ÂµM DNR or 1 ÂµM DNR + 20ÂµM VAS 2870. RNAs were purified from 3 independent experiments and used to probe Affymetrix Human Gene 2.0 ST Genechips

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H3K9 acetylation and di-methylation changes in HL-60 cells following treatment with different compounds

Project description:We investigate the effects of GCN5 and LSD1 inhibition in acute myeloid leukemia. Therefore, we characterized acetylation and di-methylation changes by ChIP-seq in AML cells (AML M2 cell line HL-60) following treatment with ATRA, MB3, GSK-LSD1 and their combinations.

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