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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE124421 | GEO | 2019/11/26

REPOSITORIES: GEO

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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

Human HL-60 Cells: all-trans retinoic acid (ATRA) vs. ATRA plus arsenic trioxide (ATO)

Project description:Transcriptional profiling of human leukemia　HL-60 cells comparing ATRA treated HL-60 cells with ATRA plus ATO. Goal was to determine the effects of ATO on ATRA induced differentiation of HL-60 cells.

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Human HL-60 Cells: all-trans retinoic acid (ATRA) vs. ATRA plus arsenic trioxide (ATO)

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Gene Expression-Based High Throughput Screening: HL-60 Cells Treated with ATRA and PMA

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 identified 8 that reliably induced the differentiation signature, and furthermore yielded functional evidence of bona fide differentiation. This data set contains HL-60 cells treated in a time course, in replicate, with 1 uM all trans retinoic acid (ATRA) and 10 nM phorbol 12-myristate 13-acetate (PMA). Also included are untreated HL-60 controls. This data set was used to select marker genes that distinguish the undifferentiated from the PMA or ATRA differentiated states. Keywords = AML Keywords = leukemia Keywords = HL-60 Keywords = chemical genomics Keywords: repeat sample

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Shotgun mass-spectrometry of HL-60 cell proteins for spectrum library development

Project description:ATRA-induced differentiation of HL-60 cells was studied using targeted mass-spectrometry including selected reaction monitoring (SRM) and parallel reaction monitoring (PRM) approach. PRM experiment was performed in time-course manner, without peptide standards usage. PRM data was inspected in Skyline 3.1 software. In order to check peptide identity we developed spectrum library based on shotgun mass-spectrometry data, which has been obtained for HL-60 cells protein samples at 0, 3, 24, 48 and 96h after ATRA treatment.

2017-11-09 | PXD006421 | Pride

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

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Inhibition of the LSD1 (KDM1A) demethylase reactivates the all-trans-retinoic acid differentiation pathway in acute myeloid leukemia [Illumina HumanHT-12 gene expression array]

Project description:All-trans-retinoic acid (ATRA) has been successfully used in therapy of acute promyelocytic leukemia (APL), a cytogenetically distinct subtype of acute myeloid leukemia (AML) but the response of non-APL AML cases to ATRA-based treatment has been poor. Here we show that, via epigenetic reprogramming, inhibitors of LSD1/KDM1 demethylase including tranylcypromine (TCP) unlocked the ATRA-driven therapeutic response in non-APL AML. LSD1 inhibition did not lead to an increase in genome-wide H3 lysine4 dimethylation (H3K4me2) but did increase H3K4me2 and expression of myeloid differentiation-associated genes. Importantly, treatment with ATRA plus TCP dramatically diminished engraftment of primary human AML cells in vivo in NOD.SCID mice, suggesting that ATRA in combination with TCP may target leukemia-initiating cells. Furthermore, initiation of ATRA plus TCP co-treatment 15 days post-engraftment of human AML cells in NOD.SCID gamma mice also revealed the ATRA plus TCP drug combination to have a potent anti-leukemic effect, which was superior to treatment with either drug alone. These data identify LSD1 as a therapeutic target and strongly suggest that it may contribute to AML pathogenesis by inhibiting the normal pro-differentiative function of ATRA, paving the way for novel combinatorial therapies of AML. Overall, 30 specimens derived from HL-60 or TEX cell line were treated with drugs and hybridized to Illumina HumanHT-12 gene expression arrays.

2012-03-14 | E-GEOD-34672 | biostudies-arrayexpress

Inhibition of the LSD1 (KDM1A) demethylase reactivates the all-trans-retinoic acid differentiation pathway in acute myeloid leukemia [ChIP-Seq]

Project description:All-trans-retinoic acid (ATRA) has been successfully used in therapy of acute promyelocytic leukemia (APL), a cytogenetically distinct subtype of acute myeloid leukemia (AML) but the response of non-APL AML cases to ATRA-based treatment has been poor. Here we show that, via epigenetic reprogramming, inhibitors of LSD1/KDM1 demethylase including tranylcypromine (TCP) unlocked the ATRA-driven therapeutic response in non-APL AML. LSD1 inhibition did not lead to an increase in genome-wide H3 lysine4 dimethylation (H3K4me2) but did increase H3K4me2 and expression of myeloid differentiation-associated genes. Importantly, treatment with ATRA plus TCP dramatically diminished engraftment of primary human AML cells in vivo in NOD.SCID mice, suggesting that ATRA in combination with TCP may target leukemia-initiating cells. Furthermore, initiation of ATRA plus TCP co-treatment 15 days post-engraftment of human AML cells in NOD.SCID gamma mice also revealed the ATRA plus TCP drug combination to have a potent anti-leukemic effect, which was superior to treatment with either drug alone. These data identify LSD1 as a therapeutic target and strongly suggest that it may contribute to AML pathogenesis by inhibiting the normal pro-differentiative function of ATRA, paving the way for novel combinatorial therapies of AML. ChIP-seq was used to study the effects of ATRA, TCP and ATRA/TCP treatment on H3K4 dimethylation. In addition to the three treatment samples, two reference samples were processed: (i) An untreated sample using the same anti-H3K4me2 antibody and an untreated sample using IgG. These five sequencing experiments were conducted using HL-60 cells and TEX cells, leading to 10 ChIP-seq samples in total.

2012-03-14 | E-GEOD-34725 | biostudies-arrayexpress

The Study of ATRA-Induced Differentiation of the HL-60 Cell Line

Project description:Shotgun mass-spectrometric experiment was performed with HL-60 cells induced to differentiation at 0, 3, 24, 48 and 96h after ATRA treatment. Obtained data has been used for label-free quantification by SPIRE platform based on spectral count. Results on proteome profiling were used for up-stream regulator search in geneXplain platform (http://genexplain.com/).

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Genome-wide maps of chromatin state ATRA treated and control HL-60 cells [ChIP-seq]

Project description:These ChIP-seq data were generated to correlate with genomic interaction data in a related Hi-C analysis.The goal of ChIP-seq are to annotate active promoter and enhancer of ATRA treated and control HL-60 cells. After ATRA induction, H3K27ac peaks distal to gene promoters showed significant changes. Those changes were correlated with interaction intensity between promoters and enhancers.

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