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Genetic and pharmacological restoration of TET2 function blocks stem cell self-renewal and progression of leukemia

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

OTHER RELATED OMICS DATASETS IN: PRJNA381792PRJNA390544PRJNA390176PRJNA381784

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE97442 | GEO | 2017/08/21

SECONDARY ACCESSION(S): PRJNA381784

REPOSITORIES: GEO

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Restoration of TET2 Function Blocks Aberrant Self-Renewal and Leukemia Progression.

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Genetic and pharmacological restoration of TET2 function blocks stem cell self-renewal and progression of leukemia

Project description:Genetic and pharmacological restoration of TET2 function blocks stem cell self-renewal and progression of leukemia

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TET2-mediated mRNA demethylation regulates leukemia stem cell homing and self-renewal.

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Tet2 loss leads to increased hematopoietic stem cell self-renewal and myeloid transformation.

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Metoclopramide treatment blocks CD93-signaling mediated self-renewal of chronic myeloid leukemia stem cells

Project description:Purpose: The goal of this study was to compare the transcriptome of FACS-purified bone marrow BL/6 (WT) or CD93-/- (KO) LSKs and BL/6 (WT) or CD93-/- (KO) LSCs. We also compared the transcriptome of FACS-purified bone marrow LSCs isolated from BL/6 mice previously treated with MCP or Veh in vivo. Methods: Transcriptomic analysis of CD93-proficient and deficient bone marrow LSKs and CML LSCs or CML LSCs upon treatment with MCP or Veh, were assessed in biological replicates using Illumina. qRT–PCR validation was performed using SYBR Green assays. Results: We mapped around 30 million sequence reads per sample to the mouse genome (GRCm38 - mm10) and identified expressed transcripts in studied samples. RNA-seq data confirmed stable expression of known housekeeping genes. Differentially expressed genes among conditions were identified with a fold change ≥1.5 and FDR p-value <0.05. Conclusions: Our study represents the first detailed transcriptome analysis of CD93-proficient and deficient bone marrow LSKs and LSCs isolated from BM of naïve and CML mice generated by RNA-seq. technology. Our results show that CD93-signaling triggers stem cell maintenance- and cell proliferation-promoting signaling pathways in CML LSCs. In addition, we showed transcriptome analysis of FACS-purified bone marrow LSCs isolated from BL/6 (WT) mice which were previously treated with MCP or Veh in vivo. Our results show that MCP treatment suppresses the stem cell maintenance- and cell proliferation-promoting signaling pathways in CML LSCs.

2021-02-07 | GSE149358 | GEO

Physioxia-induced downregulation of Tet2 in hematopoietic stem cells contributes to enhanced self-renewal.

Project description: Not available

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TET2 deficiency maintains leukemia stem cell self-renewal and subverts tumor immunity [model 1]

Project description:To investigate the function of TET2 in the development of acute myeloid leukemia (AML), we performed gene expression profiling analysis using data obtained from RNA-seq of AML cells carrying Tet2+/+ versus Tet2-/-.

2023-06-23 | GSE206456 | GEO

TET2 deficiency maintains leukemia stem cell self-renewal and subverts tumor immunity [model 2]

2023-06-23 | GSE206457 | GEO

Decreased vitamin C uptake mediated by SLC2A3 promotes leukaemia progression and impedes TET2 restoration.

Project description: Not available

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NRASG12V mediates leukemia self renewal [Microarray]

Project description:Mutant RAS oncoproteins activate signaling molecules that drive oncogenesis in multiple human tumors including acute myelogenous leukemia (AML). However, the specific function of these pathways in AML is unclear. To elucidate the downstream functions of activated NRAS in AML, we employed a murine model of AML harboring Mll-AF9 and NRASG12V. We found that NRASG12V enforced leukemia self-renewal gene expression signatures and was required to maintain an MLL-AF9 and MYB-dependent gene expression program. In a multiplexed analysis of RAS-dependent signaling intermediates, the leukemia stem cell compartment was preferentially sensitive to RAS withdrawal. Use of RAS-pathway inhibitors showed that NRASG12V maintained leukemia self-renewal through mTOR and MEK pathway activation, implicating these pathways as potential targets for cancer stem cell-specific therapies. Mice harboring NRASG12V/Mll-AF9 AML were treated with doxycyline to abolish NRASG12V expression. Leukemia samples were harvested at 12 hour intervals after doxycyline treatment. RNA was extracted from these samples and submitted for gene expression microarray analysis

2014-11-16 | E-GEOD-49038 | biostudies-arrayexpress

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