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Histone demethylase KDM4A-mediated promotion of PAF1/NFATC2 expression is required for oncogenesis in MLL-AF9 acute myeloid leukemia [RNA-seq]

ABSTRACT: In this study we identified the histone demethylase KDM4A as an essential and selective regulator of AML oncogenic potential. RNAseq was used to follow the changes in gene expression following KDM4A knockdown in MLL-AF9 human AML THP-1 cells

ORGANISM(S): Homo sapiens

PROVIDER: GSE125374 | GEO | 2021/01/17

REPOSITORIES: GEO

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Histone demethylase KDM4A-mediated promotion of PAF1/NFATC2 expression is required for oncogenesis in MLL-AF9 acute myeloid leukemia [ChIP-seq]

Project description:In this study we identified the histone demethylase KDM4A as an essential and selective regulator of AML oncogenic potential. ChIPseq was used to identify KDM4A bound genes and follow changes in H3K9me2/3 and H3K27me3 following KDM4A knockdown in MLL-AF9 human AML THP-1 cells

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Histone demethylase KDM4A-mediated promotion of PAF1/NFATC2 expression is required for oncogenesis in MLL-AF9 acute myeloid leukemia

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

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Histone demethylase KDM4A-mediated promotion of PAF1/NFATC2 expression is required for oncogenesis in MLL-AF9 acute myeloid leukemia

Project description:Histone demethylase KDM4A-mediated promotion of PAF1/NFATC2 expression is required for oncogenesis in MLL-AF9 acute myeloid leukemia

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Project description:In this study we identify genes, that are bound by Kdm4a and Kdm4c in L-GMP cells. MLL-AF9 transformed L-GMP cell lines conditional knockout for Kdm4a, b and c, were derived from leukemic mice. The cells were treated with 4-hydroxytamoxifen and chromatin was prepared from untreated cells (Ctrl) and cells treated for 96hr.

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Identification of Kdm4a, b and c target genes in MLL-AF9 transformed mouse GMPs (L-GMP) [gene expression]

Project description:In this study we identify genes, that are deregulated in Kdm4a, b and c triple knockout L-GMP cells compared WT L-GMP cells. Four MLL-AF9 transformed L-GMP cell lines conditional knockout for Kdm4a, b and c, were derived from leukemic mice. The cells were treated with 4-hydroxytamoxifen and total RNA was prepared from 0h, 48h and 96h time points.

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Histone demethylase KDM4A-mediated promotion of PAF1/NFATC2 expression is required for oncogenesis in MLL-AF9 acute myeloid leukemia [RNA-seq]

Project description:Histone demethylase KDM4A-mediated promotion of PAF1/NFATC2 expression is required for oncogenesis in MLL-AF9 acute myeloid leukemia [RNA-seq]

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Histone demethylase KDM4A-mediated promotion of PAF1/NFATC2 expression is required for oncogenesis in MLL-AF9 acute myeloid leukemia [ChIP-seq]

Project description:Histone demethylase KDM4A-mediated promotion of PAF1/NFATC2 expression is required for oncogenesis in MLL-AF9 acute myeloid leukemia [ChIP-seq]

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POLR2M-mediated paused transcription silences tumor suppressor MIR139 in MLL-AF9 AML

Project description:MIR139 is a critical tumor suppressor and commonly silenced in human cancer, including acute myeloid leukemia (AML). Here, we found that depletion of identified MIR139 targets affects AML outgrowth. We unraveled the mechanism of MIR139 gene inactivation in AML expressing the Mixed-Lineage Leukemia (MLL)-AF9 oncogene. Epigenetic analyses revealed two well-conserved putative enhancer regions in close proximity of transcriptional start sites (TSS) of MIR139. These regions were silenced by the Polycomb-Repressive Complex-2 (PRC2) downstream of MLL-AF9. Genomic deletion of these regions abolished MIR139 transcriptional regulation in normal and oncogenic conditions. Genome-wide knockout screens revealed the transcriptional pausing factor of RNA Polymerase-II, POLR2M, as a critical MIR139-silencing factor. Furthermore, direct POLR2M binding to the MIR139 TSS induced paused transcription, which was abrogated upon PRC2 inhibition. We present evidence for an oncogenic POLR2M-mediated MIR139 silencing mechanism, downstream of MLL-AF9 and PRC2. Together, our findings highlight the importance of POLR2M-mediated paused transcription in AML.

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Controlled MLL-AF9 Expression in Human Induced Pluripotent Stem Cells Reveals MLL-AF9-specific Oncogene Program [hiMLLAF9_scRNAseq]

Project description:A t(9;11)(p22;q23) translocation produces the MLL-AF9 fusion protein, which is found in up to 25% of de novo AML cases in children. Despite major advances, obtaining a comprehensive under-standing of context-dependent MLL-AF9-mediated gene programs during early hematopoiesis is challenging. Here, we generated a human inducible pluripotent stem cell (hiPSC) model with a doxycycline dose-dependent MLL-AF9 expression. We exploited MLL-AF9 expression as an onco-genic hit to uncover epigenetic and transcriptomic effects on iPSC-derived hematopoietic develop-ment and the transformation into (pre-)leukemic states. In doing so, we observed a disruption in early myelomonocytic development. Accordingly, we identified gene profiles that were consistent with primary MLL-AF9 AML and uncovered high-confidence MLL-AF9-associated core genes that are faithfully represented in primary MLL-AF9 AML, including known and presently unknown factors. Using single-cell RNA-sequencing, we identified an increase of CD34 expressing early hematopoietic progenitor-like cell states as well as granulocyte-monocyte progenitor-like cells upon MLL-AF9 activation. Our system allows for careful chemically controlled and stepwise in vitro hiPSC-derived differentiation under serum-free and feeder-free conditions. For a disease that cur-rently lacks effective precision medicine, our system provides a novel entry-point into exploring po-tential novel targets for personalized therapeutic strategies.

2023-05-03 | GSE217014 | GEO

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