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Expression data from WT HL60 cells

ABSTRACT: We used the microarray analysis to detail the gene expression profile from the leukemic cell line HL-60

ORGANISM(S): Homo sapiens

PROVIDER: GSE32153 | GEO | 2012/12/01

SECONDARY ACCESSION(S): PRJNA154947

REPOSITORIES: GEO

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Expression data from WT HL60 cells

Project description:We used the microarray analysis to detail the gene expression profile from the leukemic cell line HL-60 Relationship between DNMT1-RNA interactions, DNA methylation and gene expression

2012-12-01 | E-GEOD-32153 | biostudies-arrayexpress

Expression data from normal peripheral blood mononuclear cells, cell lines K562 and HL60

Project description:We did microarray to compare the gene expression profile of peripheral blood mononuclear cells (PBMC from normal volunteer) and two leukemic cell lines that is K562 (Chronic myelogenous leukemia cell line), HL60 (Promyelocytic leukemia cell line) in order to find differentially expressed genes in these samples.

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Staphylococcus aureus lipoteichoic acid-stimulated undifferentiated and neutrophil-like differentiated HL-60 cells

Project description:HL-60 is a human promyelocytic leukemia cell line and differentiated HL-60 is an alternative to human primary neutrophils. The transcriptomic profile of undifferentiated HL-60 and dimethyl sulfoxide-differentiated HL-60 were determined at 4 and 24 hours after stimulation with high and low concentrations of Staphylococcus aureus lipoteichoic acids.

2023-12-15 | GSE239859 | 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).

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Gene Expression Profiling Unveils the Temporal Dynamics of CIGB-300-Regulated Transcriptome in AML Cells

Project description:Transcriptomic profile study comparing human acute leukemia derived cell lines HL-60 and OCI-AML3 treated with the antitumoral peptide CIGB-300 at 30min and at 3h. CIGB-300 is an antitumoral peptide that blocks CK2 phospho-acceptor sites on their substrates but it also binds to CK2α catalytic subunit. This peptide has demonstrated their antiproliferative effects on different models including acute leukemia cells and also their antitumoral action in animal models and in clinical assays. We performed a Clariom S HT microarray gene RNA expression profiling to study the molecular events supporting the anti-leukemic effect of CIGB-300 peptide on HL-60 and OCI-AML3 cell lines.

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Gene expression profiles during the process of differentiation of HL-60 cells into neutrophils [HL60]

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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.

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Identification of genes differentially expressed in HAX1-deficient HL-60 cells

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