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Novel Inhibitors of the Histone-Methyltransferase DOT1L Show Potent Antileukemic Activity in Patient-derived Xenografts (RNA-seq dataset)

ABSTRACT: Using 3-end RNA-seq followed by digital gene expression analyses we assessed genes that change expression upon treatment with the DOT1L-methyltransferase inhibitors EPZ5676 and the novel drug "compound 10"

ORGANISM(S): Homo sapiens

PROVIDER: GSE149184 | GEO | 2020/06/01

REPOSITORIES: GEO

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Novel Inhibitors of the Histone-Methyltransferase DOT1L Show Potent Antileukemic Activity in Patient-derived Xenografts (ChIP-seq dataset)

Project description:using ChIP-seq we examined Chromatin occupancy of the MLL-fusion complex members Menin and DOT1L after treatment with DOT1L methyltransferase inhibitors EPZ5676 and the novel compounds "compound 10" and "compound 11" as well as with the Menin-inhibitor VTP50469 in MOLM13 cells. Furthermore we used ChiP-seq to quantify the loss of H3K79me2 (histone mark deposited by DOT1L) after treatment with the DOT1L inhibitors EPZ5676 and "compound 10" in MOLM13 and RS4,11 cells.

2020-06-01 | GSE149183 | GEO

Novel inhibitors of the histone methyltransferase DOT1L show potent antileukemic activity in patient-derived xenografts.

Project description: Not available

| S-EPMC8209563 | biostudies-literature

Novel Inhibitors of the Histone-Methyltransferase DOT1L Show Potent Antileukemic Activity in Patient-derived Xenografts

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

2020-06-01 | GSE149185 | GEO

Novel Inhibitors of the Histone-Methyltransferase DOT1L Show Potent Antileukemic Activity in Patient-derived Xenografts

Project description:Novel Inhibitors of the Histone-Methyltransferase DOT1L Show Potent Antileukemic Activity in Patient-derived Xenografts

| PRJNA627609 | ENA

Novel Inhibitors of the Histone-Methyltransferase DOT1L Show Potent Antileukemic Activity in Patient-derived Xenografts (ChIP-seq dataset)

Project description:Novel Inhibitors of the Histone-Methyltransferase DOT1L Show Potent Antileukemic Activity in Patient-derived Xenografts (ChIP-seq dataset)

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Novel Inhibitors of the Histone-Methyltransferase DOT1L Show Potent Antileukemic Activity in Patient-derived Xenografts (RNA-seq dataset)

Project description:Novel Inhibitors of the Histone-Methyltransferase DOT1L Show Potent Antileukemic Activity in Patient-derived Xenografts (RNA-seq dataset)

| PRJNA627611 | ENA

RNAsequencing of DOT1L inhibitor EPZ5676 treated ALDH1+ and ALDH1- cell populations

Project description:Global gene expression profiles obtained after treating cells with DOT1L inhibitor, EPZ5676

2022-01-29 | GSE194434 | GEO

DOT1L-mediated Murine Neuronal Differentiation associates with H3K79me2 Accumulation and preserves SOX2-Enhancer Accessibility

Project description:To study whether acute inhibition of DOT1L induces global chromatin states alterations, we profile and compare the transcriptome, chromatin accessibility and epigenome (H3K4me3, H3K4me1, H3K27ac, H3K27me3, H3K36me3, H3K9me3, H3K79me2) of mESC and ES-derived NPC, treated with DMSO or EPZ5676.

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Inhibition of DOT1L increases osteoclast fusion and resorption and aggravates bone loss

Project description:Osteoclasts are absorptive cells and play a critical role in homeostatic bone remodeling and pathological bone resorption. Emerging evidence suggests an important role for epigenetic regulation of osteoclastogenesis. In this study, we investigated the role of DOT1L, which regulates gene expression epigenetically by histone H3K79 methylation during osteoclast formation. DOT1L and H3K79me2 levels were upregulated during osteoclast differentiation. Small molecule inhibitor- (EPZ5676 or EPZ004777) or short hairpin RNA-mediated reduction in DOT1L expression promoted osteoclast differentiation and resorption. DOT1L inhibition also increased osteoclast area and accelerated bone mass reduction in a mouse ovariectomy (OVX) model of osteoporosis. DOT1L inhibitors did not alter osteoblast differentiation in vitro and in vivo. Proteomics data, together with bioinformatics analysis, revealed that DOT1L inhibition altered reactive oxygen species (ROS) generation, autophagy activation, and cell fusion-related protein expression. ROS generation increased, and autophagy activation and cell migration ability enhancement were verified subsequently by flow cytometry and transwell migration assays. DOT1L inhibition increased NFATc1 nuclear translocation and NF-κB activation and strengthend osteoclast fusion and expression of resorption-related protein CD9, and MMP9 in osteoclasts derived from RAW264.7. Our findings support a new mechanism of DOT1L-mediated H3K79me2 epigenetic regulation of osteoclast differentiation, implicating DOT1L as a new therapeutic target for osteoclast dysregulation-induced disease.

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Antitumor effects of DOT1L inhibition in retinoblastoma

Project description:Epigenetic dysregulation is one of the molecular mechanisms contributing to retinoblastoma (RB) development. Consistent with this notion, human RB tumors show an aberrant expression of many chromatin regulators whereas normal retina or nontumoral retinal tissues do not have any detectable expression of such proteins. Among the chromatin regulators found to be misregulated in RB, this study focuses on a histone methyltransferase DOT1L to assess the therapeutic potential of its targeting for RB treatment. We found that pharmacological inhibition of DOT1L has growth-inhibitory effects on RB cells by itself and also can sensitize RB cells to standard chemotherapeutic drugs by inducing more robust apoptotic cell death when cells are subjected to combination treatments. To understand the molecular mechanisms underlying the growth inhibition and chemosensitization of RB cells upon DOT1L inhibition, we performed the gene expression profiling in Y79 cells treated with a DOT1L inhibitor EPZ5676 in comparison with a vehicle control by RNA-sequencing to identify differentially expressed genes. Our RNA-seq results revealed that DOT1L inhibition downregulates several genes which are known to be misregulated in cancers, including HMGA2.

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