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Gene expression signature of MYB-GATA overexpression plus GATA1 down regulation in undifferentiated or differentiated UT7 cells

ABSTRACT: Acute basophilic leukemia is a rare subtype of acute myeloblastic leukemia. We recently described a recurrent t(X;6)(p11;q23) translocation occurring in male infants with acute basophilic leukemia, generating a MYB-GATA1 fusion gene. To better understand the role of MYB-GATA1 in the leukemogenesis of acute basophilic leukemias, we expressed this chimeric transcription factor in the UT-7 cell line under normal or differentiating conditions. A gene expression analysis revealed 9 genes deregulated by both MYB-GATA1 and the basophilic differentiation. Three of these genes (CCL23, IL1RL1 and NTRK1) were also increased by MYB-GATA1 in CD34-positive cells, as indicated by quantitative RT-PCR.

ORGANISM(S): Homo sapiens

PROVIDER: GSE72913 | GEO | 2017/05/31

SECONDARY ACCESSION(S): PRJNA295320

REPOSITORIES: GEO

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Gene expression signature of MYB-GATA overexpression plus GATA1 down regulation in undifferentiated or differentiated UT7 cells

Project description:Acute basophilic leukemia is a rare subtype of acute myeloblastic leukemia. We recently described a recurrent t(X;6)(p11;q23) translocation occurring in male infants with acute basophilic leukemia, generating a MYB-GATA1 fusion gene. To better understand the role of MYB-GATA1 in the leukemogenesis of acute basophilic leukemias, we expressed this chimeric transcription factor in the UT-7 cell line under normal or differentiating conditions. A gene expression analysis revealed 9 genes deregulated by both MYB-GATA1 and the basophilic differentiation. Three of these genes (CCL23, IL1RL1 and NTRK1) were also increased by MYB-GATA1 in CD34-positive cells, as indicated by quantitative RT-PCR. Two independant experiments (A and S) were performed. For each experiment, UT7 cells were transduced with two lentivirus: a lentivirus carrying the MYB-GATA1 (or a control) coding sequence, and a lentivirus carrying a GATA1 (or control) shRNA. Cells transduced with both lentiviruses were selected, and kept in culture under standard or differentiating conditions for 7 days before RNA extraction.

2016-09-01 | E-GEOD-72913 | biostudies-arrayexpress

Next generation sequencing analysis of transcriptomes at different timepoints after chlorprothixene treatment in NB4 and Kasumi-1 cells

Project description:To understand the mechanisms of chlorprothixene in acute myeloblastic leukemia (AML) therapy, gene expression changes of NB4 and Kasumi-1cells after chlorprothixene treatment were analyzed by RNA-seq

2019-12-23 | GSE124316 | GEO

MLL rearrangements in pediatric ALL and AML: MLL specific and lineage specific signatures

2009-07-22 | GSE14062 | GEO

Expression Profiling of Erythroid Progenitors After MYB shRNA Knockdown

Project description:MYB plays a critical role as a regulator of erythropoieisis. We have shown that MYB silences epsilon and gamma-globin expression in erythroid progenitors. We here examine erythroid cells at the basophilic erythroblast stage of differentiation with MYB shRNA or control lentiviral transduction prior to differentiation. We have cultured CD34 cells and transduced the cells with lentiviruses harboring shRNAs targeting MYB or controls and then allowed the cells to differentiate down the erythroid lineage. At the basophilic erythroblast stage of differentiation, the cells were harvested and total RNA was extracted. This was used to hybridize to Affymetrix expression arrays using the HG-U133 Plus 2.0 platform to ascertain expression differences that occur with the knockdown of MYB.

2011-01-03 | E-GEOD-25678 | biostudies-arrayexpress

Inactivation of the nuclear interacting SET domain protein 1 (NSD1) impairs GATA1-regulated erythroid differentiation and causes erythroleukemia

Project description:Nuclear receptor binding SET domain protein 1 (NSD1) is recurrently mutated in human cancers including acute leukemia. We found that NSD1 knockdown altered erythroid clonogenic growth of human CD34+ hematopoietic cells. Ablation of Nsd1 in the hematopoietic system induced a transplantable erythroleukemia in mice. Despite abundant expression of the transcriptional master regulator GATA1, in vitro differentiation of Nsd1-/- erythroblasts was majorly impaired associated with reduced activation of GATA1-induced targets, while GATA1-repressed target genes were less affected. Retroviral expression of wildtype Nsd1, but not a catalytically-inactive Nsd1N1918Q SET-domain mutant induced terminal maturation of Nsd1-/- erythroblasts. Despite similar GATA1 levels, exogenous Nsd1 but not Nsd1N1918Q significantly increased GATA1 chromatin occupancy and target gene activation. Notably, Nsd1 expression reduced the association of GATA1 with the co-repressor SKI, and knockdown of SKI induced differentiation of Nsd1-/- erythroblasts. Collectively, we identified the NSD1 methyltransferase as a novel regulator of GATA1-controlled erythroid differentiation and leukemogenesis.

2020-04-08 | PXD017657 | Pride

Expression Profiling of Erythroid Progenitors After MYB shRNA Knockdown

2011-01-03 | GSE25678 | GEO

Transcription profiling of human lymphoblastic and myeloblastic leukemia samples with and without MLL rearrangements specific and lineage specific signatures

Project description:Gene expression analysis identified a MLL translocation-specific signature of differentially expressed genes discriminating ALL and AML with and without MLL rearrangements. Gene expression signatures of acute lymphoblastic and myeloblastic leukemia samples with and without MLL rearrangements were analyzed using paired supervised analyses. Experiment Overall Design: ALL and AML patients with and without MLL rearrangements have been studied using paired class comparison (SAM) and class prediction (PAM) analyses.

2009-08-07 | E-GEOD-14062 | biostudies-arrayexpress

Targeting CDK6 and BCL2 exploits the "MYB Addiction" of Ph+ acute lymphoblastic leukemia

Project description:Transcriptome analysis of two Ph+ acute lymphoblastic leukemia cell lines after doxycycline induced silencing of MYB. Current treatment options for Ph+ acute lymphoblastic leukemia (ALL) do not result in long term remission. MYB transcription factor has been shown to be selectively important for Ph+ ALL cell survival and proliferation however the mechanisms for this oncogene addiction are poorly understood and no bona-fide MYB inhibitors currently exist. To overcome these limitations, we analyzed the transcriptome of MYB silenced Ph+ ALL in search for genes regulated by MYB that could serve as potential pharmacological targets. We observed that among MYB-regulated genes, those involved in cell cycle regulation are significantly over-represented. We found that CDK6 and BCL2 are MYB targets pivotal for MYB dependent regulation of proliferation and survival respectively. Furthermore, their inhibition suppresses leukemia growth in vitro and in vivo thus providing a potential treatment approach for patients that fails or do not respond to conventional treatments.

2018-01-17 | GSE105826 | GEO

Homo sapiens

Project description:Peptidomimetic blockade of MYB in acute myeloid leukemia [MYB ChIP-seq]

| PRJNA369116 | ENA

AML mouse models

Project description:This SuperSeries is composed of the following subset Series: GSE30745: Expression data from murine acute myeloid leukemia (AML) cells following shRNA-mediated suppression of Myb GSE30746: Expression data from murine Tet-off MLL-AF9/Ras acute myeloid leukemia cell lines following withdrawal of MLL-AF9 Refer to individual Series

2011-08-04 | E-GEOD-30747 | biostudies-arrayexpress

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