Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

16 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Expression profiling of myeloid leukemia cell treated with vibsanine A, PMA and ATRA

ABSTRACT: All-trans retinoic acid (ATRA)-based differentiation therapy has achieved success with the treatment of acute promyelocytic leukemia (APL), a unique subtype of acute myeloid leukemia (AML). However, other subtypes of AML display resistance to ATRA-based treatment. Here, we demonstrate that a novel natural vibsane-type diterpenoid vibsanine A promotes the differentiation of myeloid leukemia cell lines and primary AML blasts. To reveal how vibsanine A function on promoting myeloid leukemia cell differentiation, we analyzed and compared the gene expression profiles in myeloid leukemia HL-60 cells treated with vibsanine A, PMA, and ATRA. HL-60 cells were treated with vibsanine A, PMA and ATRA for 6 hours or longer up to 24 hours. Gene expression profiling was conducted

ORGANISM(S): Homo sapiens

SUBMITTER: Yu Zuyin

PROVIDER: E-GEOD-78734 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Expression profiling of myeloid leukemia cell treated with vibsanin A, PMA and ATRA

Project description:All-trans retinoic acid (ATRA)-based differentiation therapy has achieved success with the treatment of acute promyelocytic leukemia (APL), a unique subtype of acute myeloid leukemia (AML). However, other subtypes of AML display resistance to ATRA-based treatment. Here, we demonstrate that a novel natural vibsane-type diterpenoid vibsanin A promotes the differentiation of myeloid leukemia cell lines and primary AML blasts. To reveal how vibsanin A function on promoting myeloid leukemia cell differentiation, we analyzed and compared the gene expression profiles in myeloid leukemia HL-60 cells treated with vibsanin A, PMA, and ATRA.

2016-02-28 | GSE78734 | GEO

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

2004-01-30 | GSE985 | GEO

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

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.

2019-11-26 | GSE124421 | GEO

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

Transcriptional response to histone deacetylase inhibitors

Project description:Histone deacetylase inhibitors are a class of drug which rapidly induce hyperacetylation of histone proteins. Here, we aimed to study the association between HDACi-induced histone acetylation and changes in gene expression. To study the early responses to HDACi treatment we treated cells with three different concentrations of two HDACi, sodium valproate (VPA) and suberoylanilide hydroxamic acid over a short timecourse. AH LCL cells were treated with 0.2mM, 1mM or 5mM valproic acid (VPA) or 0.5, 2.5 or 12.5µM suberoylanilide hydroxamic acid (SAHA). GM12878 cells were treated with 1mM VPA. Samples were collected at 0, 30, 60 and 120 minutes. All experiments were carried out in triplicate. One replicate of AH LCL, 0.2mM VPA, 30min and one replicate of AH LCL, 5mM VPA, 30min were eliminated as outliers

2015-08-31 | E-GEOD-65297 | biostudies-arrayexpress

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

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

Transcription profiling of human acute myeloid leukemia cells to identify compounds inducing the differentiation of acute myeloid leukemia cells

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 SuperSeries is composed of the following subset Series:; GSE976: Gene Expression-Based High Throughput Screening: APL Treatment with Candidate Compounds; GSE982: Gene Expression-Based High Throughput Screening: HL-60 Cell Treatment with Candidate Compounds; GSE983: Gene Expression-Based High Throughput Screening: Primary Patient AML Blasts, Normal Neutrophils, and Normal Monocytes; GSE985: Gene Expression-Based High Throughput Screening: HL-60 Cells Treated with ATRA and PMA Experiment Overall Design: Refer to individual Series

2007-09-20 | E-GEOD-995 | biostudies-arrayexpress

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.

2015-03-31 | GSE67420 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data