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IDENTIFICATION AND FUNCTIONAL DEMONSTRATION OF A FETAL-SPECIFIC AXIS THAT POTENTLY SUPPRESSES MLL-FUSION DRIVEN MURINE AML miRNA-seq [WT vs ME]

ABSTRACT: LIN28B suppresses MLL-ENL driven AML. The tumor suppressor effects of LIN28B are largely driven by positive regulation of MYBBP1A.

ORGANISM(S): Mus musculus

PROVIDER: GSE201371 | GEO | 2023/04/28

REPOSITORIES: GEO

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IDENTIFICATION AND FUNCTIONAL DEMONSTRATION OF A FETAL-SPECIFIC AXIS THAT POTENTLY SUPPRESSES MLL-FUSION DRIVEN MURINE AML RNA-seq [L28BME vs ME]

Project description:LIN28B suppresses MLL-ENL driven AML. The tumor suppressor effects of LIN28B are largely driven by positive regulation of MYBBP1A.

2023-04-28 | GSE201370 | GEO

IDENTIFICATION AND FUNCTIONAL DEMONSTRATION OF A FETAL-SPECIFIC AXIS THAT POTENTLY SUPPRESSES MLL-FUSION DRIVEN MURINE AML miRNA-seq [L28BME vs ME]

Project description:LIN28B suppresses MLL-ENL driven AML. The tumor suppressor effects of LIN28B are largely driven by positive regulation of MYBBP1A.

2023-04-28 | GSE201372 | GEO

IDENTIFICATION AND FUNCTIONAL DEMONSTRATION OF A FETAL-SPECIFIC AXIS THAT POTENTLY SUPPRESSES MLL-FUSION DRIVEN MURINE AML

Project description:MLL-rearrangements (MLL-r) are recurrent genetic events in acute myeloid leukemia (AML) and frequently associate with poor prognosis. In infants, MLL-r have been suggested to be sufficient to drive transformation. However, despite the prenatal origin of MLL-r, the incidence of congenital leukemia is very low with transformation usually occurring postnatally. The influence of prenatal signals on leukemogenesis, such as those mediated by the fetal-specific RNA binding protein LIN28B, remains controversial. Here, using a dual-transgenic mouse model that co-express MLL-ENL and LIN28B, we investigated the impact of LIN28B on AML. We show that LIN28B impedes the progression of MLL-r AML through a compromised leukemia initiating cell activity and a suppression of MYB signaling. Mechanistically, rather than involving the well-studied Lin28B-let7 miR axis, we found that LIN28B directly bound MYBBP1A mRNA, a co-repressor of MYB, and that positively correlated with MYBBP1A protein levels. Overexpression of MYBBP1A in MLL-ENL driven leukemogenesis largely phenocopied the tumor suppressor effects of LIN28B. Thereby, our work proposes that the developmentally-restricted expression of LIN28B during fetal development provides a protection against MYB-dependent AML.

2023-02-08 | GSE201083 | GEO

Protein Interactions of 7 MLL-fusion Proteins

Project description:MLL-fusions represent a large group of leukemia drivers, whose diversity originates from the vast molecular heterogeneity of C-terminal fusion partners of MLL protein. While studies of selected MLL-fusions have revealed critical molecular pathways, unifying mechanisms across all MLL-fusions remain poorly understood. We present the first comprehensive survey of protein-protein interactions of seven distantly related MLL-fusion proteins: MLL-AF1p, MLL-AF4, MLL-AF9, MLL-CBP, MLL-EEN, MLL-ENL and MLL-GAS7.

2018-05-25 | PXD009338 | Pride

Expression data from conditionally immortalized MLL-AF9 and MLL-ENL hematopoietic progenitor cells following loss of MLL-fusion oncogene

Project description:Chromosomal translocations encoding the MLL-AF9 and MLL-ENL fusion transcription factors are prevalent in infant acute leukaemia and therapy-related leukaemia. In order to conditionally express the MLL-fusion oncogene in primary haematopoietic progenitor cells (HPC), retroviral delivery of the Tet-off expression system was used (Horton et al., Cancer Res, 2005). Treatment of the conditional cells with Doxycycline caused a decrease in MLL-AF9/ENL mRNA and protein expression, and resulted in terminal differentiation of the cells. By analysing global changes in gene expression after treatment of cells with Doxycycline we were able to identify a number of potential transcriptional target genes of the MLL-AF9 and MLL-ENL fusion oncogenes.

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Quantitative cellular proteome analysis of Fetal- and Adult-Derived MLL-Rearranged Leukemia

Project description:Infant and adult MLL-rearranged (MLLr) leukemia represents a disease with few treatment options and a dismal prognosis. Here, we present an in-depth proteomic characterization of in utero-initiated and adult-onset MLLr leukemia in a mouse model of MLL-ENL-mediated leukemogenesis. We characterize early proteomic events of MLL-ENL-mediated transformation in fetal and adult progenitors.

2024-04-02 | PXD042249 | Pride

IDENTIFICATION AND FUNCTIONAL DEMONSTRATION OF A FETAL-SPECIFIC AXIS THAT POTENTLY SUPPRESSES MLL-FUSION DRIVEN MURINE AML

Project description:IDENTIFICATION AND FUNCTIONAL DEMONSTRATION OF A FETAL-SPECIFIC AXIS THAT POTENTLY SUPPRESSES MLL-FUSION DRIVEN MURINE AML

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Transcriptomic profiling of MLL-ENL and delta YEATS mutant

Project description:To investigate the contribution of ENL YEATS domain and downstream sequences in MLL-ENL leukemogenesis program, we generated MLL-ENL and MLL-ENL ∆YEATS (ENL aa372-559) cell lines by retrovirally introducing these constructs into lineage negative hematopoietic stem and progenitor cells (HSPCs).

2023-02-27 | GSE211523 | GEO

MLL Fusion Proteins Preferentially Regulate a Small Set of Wild Type MLL Target Genes in the Leukemic Genome

Project description:MLL encodes a histone methyltransferase that is critical in maintaining gene expression during embryonic development and hematopoiesis. 11q23 translocations encode chimeric MLL fusions that act as potent drivers of acute leukemia. However, it remains unclear what portion of the leukemic genome is under the direct control of the MLL fusion protein. By comparing patient-derived leukemic cell lines, we find that MLL fusion-bound genes are a small subset of that recognized by wild-type MLL. In an inducible MLL-ENL cellular model, binding of the MLL fusion protein and changes in H3K79 methylation are limited to a specific portion of the genome, whereas wild-type MLL distributes to a much larger set of gene loci. Surprisingly, among 223 MLL fusion-bound genes, only 12 demonstrate a significant increase in mRNA expression upon induction of the fusion protein. In addition to Hoxa9 and Meis1, this includes Eya1 and Six1 which comprise a heterodimeric transcription factor important in several developmental pathways. We show that Eya1 has the capacity to immortalize hematopoietic progenitor cells in vitro and collaborates with Six1 in hematopoietic transformation assays. Altogether, our data suggest that MLL fusions contribute to the development of acute leukemia through direct activation of a small set of target genes. We explored an inducible MLL-ENL cellular model, which was obtained from Dr. Robert Slany (University Erlangen, Germany). We wished to examine the differential expressed genes that are bound by MLL wild type (No 4-OHT) and fusion (4-OHT) proteins, combinding the ChIP-chip data to explore the potential MLL fusion-regulated genes.

2011-04-28 | E-GEOD-24794 | biostudies-arrayexpress

Runx1 deficiency effect on MLL-ENL cells

Project description:To identify the target genes of Runx1 in MLL fusion leukemia, we performed microarray analysis using control and Runx1-deficient MLL-ENL leukemia cells. Runx1 intact and excised bone marrow cells were transduced with MLL-ENL and transplanted into congenic mice. Leukemic cells were harvested from moribund mice, and gene expression was compared using 3 independent leukemia cells for each genotype.

2013-06-30 | E-GEOD-47402 | biostudies-arrayexpress

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