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G9a-dependent gene expression in mouse AML cells

ABSTRACT: The methyltransferase G9a was found to play a role in the disease progression of a murine model of AML. Mouse HSPCs were transformed with HoxA9/Meis1 and treated with G9a/GLP inhibitor UNC0638. We used microarrays to detail the global program of gene expression that depends on the methyltransferase activity of G9a in murine AML cells.

ORGANISM(S): Mus musculus

SUBMITTER: Bernhard Lehnertz

PROVIDER: E-GEOD-53894 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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The methyltransferase G9a regulates HoxA9-dependent transcription in AML.

Lehnertz Bernhard B Pabst Caroline C Su Le L Miller Michelle M Liu Feng F Yi Lin L Zhang Regan R Krosl Jana J Yung Eric E Kirschner Jeanette J Rosten Patty P Underhill T Michael TM Jin Jian J Hébert Josée J Sauvageau Guy G Humphries R Keith RK Rossi Fabio M FM

Genes & development 20140201 4

Chromatin modulators are emerging as attractive drug targets, given their widespread implication in human cancers and susceptibility to pharmacological inhibition. Here we establish the histone methyltransferase G9a/EHMT2 as a selective regulator of fast proliferating myeloid progenitors with no discernible function in hematopoietic stem cells (HSCs). In mouse models of acute myeloid leukemia (AML), loss of G9a significantly delays disease progression and reduces leukemia stem cell (LSC) frequen ...[more]

PMID: 24532712

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G9a-dependent gene expression in mouse AML cells

Project description:The methyltransferase G9a was found to play a role in the disease progression of a murine model of AML. Mouse HSPCs were transformed with HoxA9/Meis1 and treated with G9a/GLP inhibitor UNC0638.

2014-01-08 | GSE53894 | GEO

HEK293T cells treated with a G9a small molecule inhibitor (UNC0638) or vehicle (DMSO), WIZ siRNA, G9a siRNA, or scrambled (control) siRNA

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Gene expression signature of HoxA9-Meis1 AML cells treated with Pyrydopyrazine

Project description:Pyrydopyrazine A2 induced in vitro the differentiation of leukemic cells (HoxA9-Meis1) into macrophages, we decided to perform a transcriptomic study in order to analyze the GM-CSF pathway regulation. We therefore compared effect with A2 to cells treated with Retinoic acid and D3 Vitamin, a combination known to induce also differentiation of leukemic cells. HoxA9-Meis1 murine AML cells were treated in vitro during 24h, with Pyrydopyrazine( A2) at 3.4μM or a combination of all-trans Retinoic Acid (RA) and 1α-hydroxy-D3 Vitamin (D3V), 10μM each. Gene expression signature was compared to untreated control. One sample was tested for each condition

2015-09-02 | E-GEOD-72635 | biostudies-arrayexpress

Expression data from G9a overexpression and knockdown lung cancer cell lines

Project description:G9a is the major mammalian H3-K9 methyltransferase that targets euchromatic regionsand is essential for murine embryogenesis . We demonstrate that G9a is endowed with methyltransferase activity to concomitantly repress the downstream effector Ep-CAM, thereby promoting the invasion step of the invasion-metastasis cascade. We used microarrays to detail the G9a regulated gene expression underlying invasion-metastasis cascade and identified distinct classes of up-regulated genes during this process. Lung adenocarcinoma cells with G9a knockdown or overexpression were selected for RNA extraction and hybridization on Affymetrix microarrays.

2011-12-31 | E-GEOD-22810 | biostudies-arrayexpress

Assesment of gene expression upon AF10 deletion in MLL-AF9 secondary leukemia

Project description:Aberrant Hox gene activation is a recurrent feature in several different types of human leukemia, including leukemias with rearrangements of the mixed lineage leukemia (MLL) gene. In this study, we demonstrate that Hox gene expression is controlled by higher degree H3K79 methylation in acute myeloid leukemia (AML). We show that the deposition of progressive H3K79 methylation states at the genomic loci of critical Hox genes is dependent on the interaction of the H3K79 methyltransferase Dot1l with Af10, a protein that is found in the Dot1l complex isolated from diverse cell types. Furthermore, abrogation of the Dot1l-Af10 interaction reverses aberrant epigenetic profiles found in the leukemia epigenome and impairs the transforming ability of mechanistically distinct AML oncogenes. Primary MLL-AF9 leukemias in the AF10 floxed background (homozygous) were transduced with MSCV-IRES-tdTomato (MIT) or the Cre recombinase expressing MIT vector, cells were sorted and injected into secondary recipient mice to generate Af10 floxed (MIT) or deleted (CRE) leukemias. BM cells fresly harvested from these leukemias were sorted for tdTomato expression and used for microarrays. BM cells from Hoxa9-Meis1 transduced primary leukemias were used for comparison.

2014-09-08 | E-GEOD-54499 | biostudies-arrayexpress

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2011-12-05 | E-GEOD-33518 | biostudies-arrayexpress

Expression data from miR-223KO and miR-223WT bone marrow cells

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2011-05-24 | E-GEOD-29453 | biostudies-arrayexpress

G9a is essential for epigenetic silencing of K+ channel genes in acute-to-chronic pain transition

Project description:AIM: We performed RNA-sequencing experiments seeking genes whose expression changed due to nerve injury. In addition, we wanted to test whether inhibition of the methyl transferase G9a/GLP, that methylates H3K9me2, could reverse those expression changes due to nerve ligation. G9a/GLP methylase was pharmacologically inhibited using UNC0638. METHOD: We generated cDNA libraries from RNA purified from DRGs obtained from Sham operated (4), SNL (4), and SNL plus UNC0638 (3) rats. We sequenced the cDNA libraries generating single end 50 bp reads on the illumina HiSeq 2500 platform. Sequencing reads were aligned to the rat genome rn4 using TopHat RESULTS: We were able to map 16876 genes, from which 2035 changed their expression values at least two fold when we compared SNL to Sham operated (pâ?¤ 0.01). There were 1205 upregulated and 832 down-regulated genes. Next, we focused on genes whose expression was either up or down-regulated 2 fold due to nerve ligation, and the values would be normalized to control level after G9a/GLP inhibito (UNC0638)r treatment. We identified 639 genes in our data set that behave this way We generated cDNA libraries from RNA purified from DRGs obtained from Sham operated (4), SNL (4), and SNL plus UNC0638 (3) rats. We sequenced the cDNA libraries generating single end 50 bp reads on the illumina HiSeq 2500 platform. Sequencing reads were aligned to the rat genome rn4 using TopHat

2015-11-02 | E-GEOD-59043 | biostudies-arrayexpress

Expression data from G9a overexpression and knockdown lung cancer cell lines

2011-12-31 | GSE22810 | GEO

Lung adenocarcinoma UNC0638 gene expression

Project description:Experiment was to determine the effects of G9a inhibition using chemical inhibitor UNC0638 on murine lung adenocarcinoma cell lines

2018-09-18 | GSE120073 | GEO

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