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Genes Differentially Expressed as a Result of Enforced EDAG Expression In 32D Cells

ABSTRACT: Erythroid differentiation-associated gene (EDAG), a hematopoietic tissue-specific transcription regulator, plays a key role in maintaining the homeostasis of hematopoietic lineage commitment. However, the mechanism and genes regulated by EDAG remain unknown.Here, we performed genome-wide parallel expression analyses of 32D cells stably transfected with EDAG.

ORGANISM(S): Mus musculus

PROVIDER: GSE18862 | GEO | 2010/07/01

SECONDARY ACCESSION(S): PRJNA121111

REPOSITORIES: GEO

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Genes Differentially Expressed as a Result of Enforced EDAG Expression In 32D Cells

Project description:Erythroid differentiation-associated gene (EDAG), a hematopoietic tissue-specific transcription regulator, plays a key role in maintaining the homeostasis of hematopoietic lineage commitment. However, the mechanism and genes regulated by EDAG remain unknown.Here, we performed genome-wide parallel expression analyses of 32D cells stably transfected with EDAG. Total RNA from the control 32D cells and 32D/EDAG cells were used to generate target cDNA, and then hybridized to 36k Mouse Genome Array Genechips, representing about 25000 characterized murine genes.

2010-07-01 | E-GEOD-18862 | biostudies-arrayexpress

Molecular variability of FLT3/ITD mutants and their impact on the differentiation program of 32D cells

Project description:FLT3 is the most frequently mutated gene in AML â up to 40% of AML harbor an activating mutation within FLT3 gene. Though AML is a relatively rare disease, such a high mutability rate, as observed with FLT3 gene, is striking. To elucidate the molecular background of this phenomenon, we have established nine unique FLT3/ITD - carrying 32D cell lines and a set of controls, and subjected them to whole genome expression analysis and 2DE LC/MS proteomics. Data obtained on this so far largest set of ITD mutants indicates that in comparison to the wild type FLT3 expressing 32D cells and transduction controls, FLT3/ITD positive cells exhibit less mature expression profiles resembling ST-HSC and MkEP/CMP/LMPP progenitors. We hypothesize that FLT3/ITD might contribute not only to the proliferative advantage of FLT3/ITD positive cells, but also to their reprogramming towards less differentiated stages, thus strengthening their malignant properties. This finding might explain the pronounced mutation rate of the aberrantly expressed FLT3 gene in AML, and, also, the inferior prognosis of FLT3/ITD positive AML patients. Moreover, the microarray data has revealed biological differences among individual ITD variants â a finding supporting the recent clinical data on the prognostic impact of the size of individual ITDs. Keywords: genetic modification Nine stable 32D cell lines harboring unique human FLT3/ITD mutants, two parental 32 cell lines, two 32D stable cell lines harboring cloning vector only, and two 32D cell lines stably expressing human wild type FLT3 were subjected to the microarray analysis.

2010-04-08 | E-GEOD-12766 | biostudies-arrayexpress

The Nup98::Nsd1 fusion gene induces CD123 expression in 32D cells

Project description:The NUP98::NSD1 fusion gene is associated with extremely poor prognosis in patients with acute myeloid leukemia (AML). NUP98::NSD1 induces self-renewal and blocks differentiation of hematopoietic stem cells, leading to leukemia development. Despite its association with poor prognosis, targeted therapy for NUP98::NSD1-positive AML is lacking, as the details of NUP98::NSD1 function are unknown. Here, we generated 32D cells (a murine interleukin-3 (IL-3)-dependent myeloid progenitor cell line) expressing mouse Nup98::Nsd1 to explore the function of NUP98::NSD1 in AML, including by comprehensive gene expression analysis. We identified two properties of Nup98::Nsd1+ 32D cells in vitro: first, Nup98::Nsd1 promoted blocking of AML cell differentiation, consistent with a previous report; second, Nup98::Nsd1 increased dependence on IL-3 for cell proliferation, due to overexpression of the alpha subunit of the IL-3 receptor (IL3-RA, also known as CD123). Consistent with our in vitro data, IL3-RA was also up-regulated in samples from patients with NUP98::NSD1-positive AML. These results highlight CD123 as a potential new therapeutic target in NUP98::NSD1-positive AML.

2022-10-25 | GSE216409 | GEO

Genome-wide C/ebpβ and Jmjd3 traget genes in 32D cells.

Project description:To characterize genome-wide C/ebpβ and Jmjd3 traget genes in 32D cells by ChIP-seq.

2018-06-13 | GSE100487 | GEO

Overexpression of miR-9 and miR-9* in 32D cells

Project description:Overexpression of miR-9 and miR-9* in 32D cells, cells grown under IL-3 conditions and miR-9 and miR-9* were introduced with retroviral vectors containing about ~150 bp up and downstream of mmu-mir-9-2. Expression was determined to find out the effect of miR-9/9*overexpression on the transcriptome level compared to introduction of empty vector control. Transcriptome levels were determined for 32D cells expressing miR-9 and miR-9* and empty vector control. Experiment performed in three independent replicates.

2012-11-01 | E-GEOD-41942 | biostudies-arrayexpress

Genes Differentially Expressed as a Result of Enforced Pokemon Expression in MCF-7 cell

Project description: Not available

| S-ECPF-GEOD-27442 | biostudies-other

Overexpression of miR-9 and miR-9* in 32D cells

2012-11-01 | GSE41942 | GEO

RNA sequencing of 32D clone 3 cells transfected with CXCR2 (pEGFP-N1-CXCR2) or an empty vector(pEGFP-N1)

Project description:Purpose: CXCR2 was transfected into 32D clone 3 cells simulating the granulocyte and macrophage progenitor cells(GMPs) to confirm the role of CXCR2 in the differentiation of GMPs to macrophage and dendritic cell progenitor cells

2019-08-21 | GSE125347 | GEO

Carfilzomib-induced reticulocytosis in patients with multiple myeloma is caused by impaired terminal erythroid maturation

Project description:Proteasome inhibition constitutes a cornerstone of multiple myeloma (MM) treatment, with bortezomib, carfilzomib and ixazomib approved for clinical use. We observed a consistent and highly significant increase in the reticulocyte count during treatment with carfilzomib-based regimens in patients with relapsed MM, an observation not made in a matched cohort of bortezomib-treated patients. As this increased reticulocytosis was neither associated with elevated hemoglobin levels nor with hemolysis, we subsequently performed in vitro experiments to unravel the underlying mechanisms of this clinical observation. While carfilzomib did not affect erythroid differentiation of CD34+ hematopoietic progenitor cells, both continuous and pulse exposure to carfilzomib significantly impaired terminal maturation of purified primary reticulocytes towards erythrocytes. These results indicate that carfilzomib significantly impairs terminal erythroid maturation, independent of erythroid commitment, expansion or differentiation. Our results report the first pharmacologically induced delay in erythroid maturation as a mechanism for carfilzomib-induced reticulocytosis in MM patients. Quantitative proteomics using LC-MS/MS were performed to assess whether carfilzomib treatment alters the protein composition of reticulocytes

2020-02-20 | PXD014353 | Pride

Genes Differentially Expressed as a Result of Enforced Pokemon Expression in MCF-7 cell

Project description:Pokmeon is an oncogenic transcription factor involved in cell growth, differentiation, and oncogenesis,but its regulatory network in breast cancer cells remians elusive . We used microarray to determine the down stream target genes of pokemon by using the MCF-7 cell line with stable ectopic expression of pokemon.

2011-02-25 | GSE27442 | GEO

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