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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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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

2022-01-08 | GSE193094 | GEO

RNA-Seq of human AML cell line, HL-60 and its mitoxantrone resistant subline HL60/MX2

Project description:Alteration in metabolic repertoire is commonly associated with resistance phenotype. Although it’s a common phenotype, not much efforts have been undertaken to design effective strategies to target the metabolic drift in such cancerous cells and especially with drug resistant properties. In our study, we identified that drug resistant AML cell line HL-60/MX2 do not follow classical Warburg effect, instead these cells exhibit drastically low levels of aerobic glycolysis. Biochemical analysis confirms reduced glucose consumption and lactic acid production by resistant population with no differences in glutamine consumption. Raman spectroscopy revealed increased lipid and cytochrome content in resistant cells which were also visualized in the form of lipid droplets by Raman mapping, electron microscopy and lipid specific staining. Gene set enrichment analysis data from both the cell lines revealed significant enrichment of lipid metabolic pathways in HL-60/MX2 cells. Further drug resistant cells possess higher mitochondrial activity and increased OXPHOS suggested the role of fatty acid metabolism as energy source which was confirmed by increased rate of fatty acid oxidation. Pharmacological inhibition of fatty acid oxidation using Etomoxir affected the colony formation ability of resistant cells and inhibition of OXPHOS using Antimycin-A increased the sensitivity of resistant cells to chemotherapeutic drug, demonstrating requirement of fatty acid metabolism and increased dependency on OXPHOS by resistant leukemic cells for tumorigenicity.

2021-01-01 | E-MTAB-8981 | biostudies-arrayexpress

SUMO2/3 CHIP-Seq in HL-60 cells treated or not with cytarabine or daunorubicine

Project description:SUMOylation, a post-translational modification of the ubiquitin family plays key roles in Acute Myeloid Leukemias response to therapies, in particular through the regulation of gene expression. We have investigated here how daunorubicine (DNR) and cytarabine (Ara-C), the two main drugs used for Acute Myeloid Leukemia treatment, affect the distribution of SUMO on chromatin in the HL-60 cell lines. We found that DNR but not Ara-C leads to a massive decrease in the presence of SUMOylated proteins on the chromatin, in particular at promoters and enhancers, where they are enriched.

2023-06-23 | GSE198985 | GEO

Epichromatin HL-60/S4

Project description:Epichromatin HL-60/S4

| PRJEB5782 | ENA

RNA-seq of 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 gene expression changes by RNA-seq in AML cells (AML M2 cell line HL-60) following treatment with ATRA, MB3, GSK-LSD1 and their combinations.

2019-11-26 | GSE124422 | GEO

microRNA array of extracellular vesicles isolated from the conditioned culture medium of HL60 cells and their chemo-resistant counterparts (HL-60/AR)

Project description:The aim of this experiment was to highlight differences in expression of microRNAs transported by extracellular vesicles between two strains of the HL-60 cell line (acute promyelocytic leukemia cell line): the chemo-sensitive strain (HL-60) and an anthracyclin-resistant strain (HL-60/AR).

2017-10-03 | E-MTAB-5551 | biostudies-arrayexpress

RNA-Seq of human AML cell line, HL-60 and its mitoxantrone resistant subline HL60/MX2

Project description:RNA-Seq of human AML cell line, HL-60 and its mitoxantrone resistant subline HL60/MX2

| PRJEB37958 | ENA

Gene Expression-Based High Throughput Screening: HL-60 Cell Treatment with Candidate Compounds

Project description:We developed a general approach to small molecule library screening called GE-HTS (Gene Expression-Based High Throughput Screening) in which a gene expression signature is used as a surrogate for cellular states and applied it to the identification of compounds inducing the differentiation of acute myeloid leukemia cells. In screening 1,739 compounds, we prioritized 15 candidate compounds (2 were already confirmed in the literature). We next evaluated the 13 remaining compounds. Eight reliably induced the differentiation signature, and furthermore yielded functional evidence of bona fide differentiation. This data set contains HL-60 cells treated in replicates of 3 with the original 13 selected candidates. It also contains 6 untreated, 6 DMSO treated, 3 ATRA treated, 3 PMA treated, and 3 1,25-dihydroxyvitamin D3 treated HL-60 controls. In addition, it contains 3 neutrophil and 3 monocyte samples from distinct normal human donors and 9 primary patient AML samples. This data set was used to evaluate the whole genome effects of the candidate compounds on HL-60 cells. Keywords = AML Keywords = leukemia Keywords = HL-60 Keywords = chemical genomics Keywords: repeat sample

2004-01-30 | GSE982 | GEO

HL-60 treated with TPA

Project description:Comparing the difference between TPA stimulated HL-60 and control

2013-05-05 | GSE29620 | GEO

mRNA-sequencing in drug-resistant acute myeloid leukemia

Project description:mRNA sequencing for AML cells(HL-60) and drug-resistant AML Cells(HL60/MX2).

2022-04-23 | GSE201095 | GEO