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Transcriptome of MV4;11 cells treated with ASH1L inhibitor AS-99

ABSTRACT: Transcriptome of MV4;11 cells treated with ASH1L inhibitor AS-99

PROVIDER: PRJNA631053 | ENA |

REPOSITORIES: ENA

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Transcriptome of MV4;11 cells treated with ASH1L inhibitor AS-99

Project description:This study describes the transcriptome profiling of MV4;11 human leukemia cells treated for 6 days with: 1) DMSO; 2) 3 µM of AS-99 ASH1L inhibitor.

2021-02-24 | GSE150085 | GEO

Analysis of MV4;11 cells treated with ASH1L inhibitor AS-99

Project description:Analysis of MV4;11 cells treated with ASH1L inhibitor AS-99

| PRJNA631052 | ENA

Genome-wide distribution of ASH1L and H3K36me2 in human MV4;11 leukemia cell line

Project description:The H3K36me2 and ASH1L levels are compared in the presence or absence of the inhibitor of the ASH1L activity.

2021-02-24 | GSE150086 | GEO

Analysis of MV4;11 cells treated with ASH1L inhibitor AS-99

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-02-24 | GSE150087 | GEO

Genome-wide distribution of ASH1L and H3K36me2 in human MV4;11 leukemia cell line

Project description:Genome-wide distribution of ASH1L and H3K36me2 in human MV4;11 leukemia cell line

| PRJNA631054 | ENA

Microarray data of human leukemia cells MV4;11 with or without IKK inhibitor treatment.

Project description:MLL fusion proteins in leukemia induce aberrant transcriptional elongation and associated chromatin perturbations, however the upstream signaling pathways and activators that recruit or retain MLL oncoproteins at initiated promoters are unknown. Through functional and comparative genomic studies, we identified an essential role for NF-kB signaling in MLL leukemia. Suppression of NF-kB led to robust anti-leukemia effects that phenocopied loss of functional MLL oncoprotein or associated epigenetic cofactors. The NF-kB subunit RELA occupies promoter regions of crucial MLL target genes and sustains the MLL-dependent leukemia stem cell program. IKK/NF-kB signaling is required for wild-type MLL and fusion protein retention and maintenance of associated histone modifications providing a molecular rationale for enhanced efficacy in therapeutic targeting of this pathway in MLL leukemias. MV4;11 cells were treated with 1ÂµM IKK inhibitor or vehicle. Each group contains triplicate samples

2013-09-19 | E-GEOD-46251 | biostudies-arrayexpress

ASH1L links histone H3 lysine 36 di-methylation to leukemia

Project description:The histone methyltransferases MLL and ASH1L are trithorax-group proteins that interact genetically through undefined molecular mechanisms to regulate developmental and hematopoietic gene expression. Here we show that the lysine 36-dimethyl mark of histone H3 (H3K36me2) written by ASH1L is preferentially bound in vivo by LEDGF, an MLL-associated protein that co-localizes with MLL, ASH1L and H3K36me2 on chromatin genome wide. Furthermore, ASH1L facilitates recruitment of LEDGF and wild type MLL proteins to chromatin at key leukemia target genes, and is a crucial regulator of MLL-dependent transcription and leukemic transformation. Conversely KDM2A, an H3K36me2 demethylase and Polycomb-group silencing protein, antagonizes MLL-associated leukemogenesis. Our studies illuminate the molecular mechanisms underlying epigenetic interactions wherein placement, interpretation and removal of H3K36me2 contribute to the regulation of gene expression and MLL leukemia, and suggest ASH1L as a target for therapeutic intervention. Investigation of multiple transcription factors and histone modification marks in MV4-11 human leukemia cells.

2016-07-01 | E-GEOD-73528 | biostudies-arrayexpress

Histone H3K36me2-specific methyltransferase ASH1L promotes the MLL-AF9-induced leukemogenesis

Project description:ASH1L and MLL1 are two histone methyltransferases that facilitate transcriptional activation during normal development. However, the roles of ASH1L and its enzymatic activity in the development of MLL-rearranged leukemias are not fully elucidated in Ash1L gene knockout animal models. In this study, we used an Ash1L conditional knockout mouse model to show that loss of ASH1L in hematopoietic progenitor cells impaired the initiation of MLL-AF9-induced leukemic transformation in vitro. Furthermore, genetic deletion of ASH1L in the MLL-AF9-transformed cells impaired the maintenance of leukemic cells in vitro and largely blocked the leukemia progression in vivo. Importantly, the loss of ASH1L function in the Ash1L-deleted cells could be rescued by wild-type but not the catalytic-dead mutant ASH1L, suggesting the enzymatic activity of ASH1L was required for its function in promoting MLL-AF9-induced leukemic transformation. At the molecular level, ASH1L enhanced the MLL-AF9 target gene expression by directly binding to the gene promoters and modifying the local histone H3K36me2 levels. Thus, our study revealed the critical functions of ASH1L in promoting the MLL-AF9-induced leukemogenesis, which provides a molecular basis for targeting ASH1L and its enzymatic activity to treat MLL-arranged leukemias.

2021-09-07 | GSE183413 | GEO

Gene expression analysis of a subcutaneous MV4;11 tumor treated with curaxin CBL0137.

Project description:The aim of this experiment was to identify how CBL0137 decreased tumor growth in a subcutaneous MV4;11 xenograft model by investigating the gene expression changes induced upon treatment.

2019-02-13 | GSE126442 | GEO

RNA-seq analysis of human KMT2A rearranged MV4;11 AML cell line treated with DOT1L and/or EZH2 inhibitor

Project description:RNA-seq analysis of human KMT2A rearranged MV4;11 AML cell line treated with DOT1L and/or EZH2 inhibitor

| PRJNA554881 | ENA