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Novel Pharmacologic Inhibition of Lysine-specific Demethylase 1 as a Potential Therapeutic for Glioblastoma [RNA-seq]

ABSTRACT: Novel Pharmacologic Inhibition of Lysine-specific Demethylase 1 as a Potential Therapeutic for Glioblastoma [RNA-seq]

PROVIDER: PRJNA1087175 | ENA |

REPOSITORIES: ENA

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Novel Pharmacologic Inhibition of Lysine-specific Demethylase 1 as a Potential Therapeutic for Glioblastoma [ChIP-seq]

Project description:Novel Pharmacologic Inhibition of Lysine-specific Demethylase 1 as a Potential Therapeutic for Glioblastoma [ChIP-seq]

| PRJNA1087174 | ENA

Novel Pharmacologic Inhibition of Lysine-specific Demethylase 1 as a Potential Therapeutic for Glioblastoma [RNA-seq]

Project description:Lysine-specific demethylase 1 (LSD1/KDM1A) is a pivotal epigenetic enzyme that contributes to several malignancies including malignant glioma. LSD1 is a flavin adenine dinucleotide dependent histone demethylase that specifically targets histone H3 lysine (K) 4 mono- (me1) and di-methylation (me2) and H3K9me1/2 for demethylation. Herein we report the development of an LSD inhibitor, S2172, which efficiently penetrates the blood-brain barrier. S2172 effectively suppresses LSD1 enzymatic activity, resulting in the depletion of cell growth both in vitro in glioma stem cells (GSCs) (mean half-maximal inhibitory concentration (IC50) of 13.8 μM) and in vivo in a GSC orthotopic xenograft mouse model. Treatment with S2172 robustly reduced the expression of the stemness-related genes MYC and Nestin in GSC cells. Consistent with this, chromatin immunoprecipitation-sequencing revealed a significant S2172-dependent alteration in H3K4me2/H3K4me3 status. Furthermore, we identified 284 newly acquired H3K4me2 peak regions after S2172 treatment, which were encompassed within super-enhancer regions. The altered H3K4me2/H3K4me3 status induced by S2172 treatment affected the expression of genes related to tumorigenesis. Our data suggest that targeting LSD1 with S2172 could provide a promising treatment option for glioblastomas, particularly due to targeting of GSC populations.

2024-11-10 | GSE261472 | GEO

Novel Pharmacologic Inhibition of Lysine-specific Demethylase 1 as a Potential Therapeutic for Glioblastoma [ChIP-seq]

2024-11-10 | GSE261471 | GEO

Inhibition of lysine-specific demethylase 1 inhibition in glioblastoma

Project description:Inhibition of lysine-specific demethylase 1 inhibition in glioblastoma

| PRJNA929532 | ENA

CpG islands recruit a histone H3 lysine 36 demethylase

Project description:This SuperSeries is composed of the following subset Series: GSE18588: CpG islands recruit a histone H3 lysine 36 demethylase [Illumina sequencing data] GSE21201: CpG islands recruit a histone H3 lysine 36 demethylase [Agilent data] Refer to individual Series

2010-04-26 | E-GEOD-21202 | biostudies-arrayexpress

Uncoupling Histone Modification Crosstalk by Engineering Lysine Demethylase LSD1

Project description:Uncoupling Histone Modification Crosstalk by Engineering Lysine Demethylase LSD1

| PRJNA1017443 | ENA

Lysine-specific demethylase 1 target genes in brown adipocytes

Project description:Lysine-specific demethylase 1 target genes in brown adipocytes

| PRJNA321978 | ENA

Targeting Lysine Demethylase 5 (KDM5) in Mantle Cell Lymphoma

Project description:Targeting Lysine Demethylase 5 (KDM5) in Mantle Cell Lymphoma

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CpG islands recruit a histone H3 lysine 36 demethylase [Illumina sequencing data]

Project description:Eukaryotic gene expression profiles are largely defined by transcription factors that recognize specific DNA sequences in gene regulatory regions and impact RNA polymerase recruitment and transcription. In addition to specific core promoter regulatory elements, up to 70% of genes in higher eukaryotes are also characterized by an overrepresentation of cytosine/guanine base pairs (CpGs) surrounding promoters and gene regulatory units. These features, called CpG islands, were identified over twenty years ago but there remains little mechanistic evidence to suggest how these enigmatic elements contribute to promoter function, with the exception that they are refractory to epigenetic silencing by DNA methylation. Here we uncover a role for CpG islands in buffering gene regulatory elements from repressive histone H3 lysine 36 methylation by directly recruiting the H3K36 specific lysine demethylase enzyme KDM2A. KDM2A is recruited to CpG islands by a zinc finger CxxC (ZF-CxxC) domain that specifically recognizes CpG DNA and is blocked by DNA methylation. This capacity to sense the epigenetic methylation state of DNA constrains KDM2A to non-methylated CpG islands. Importantly, these observations suggest CpG islands may function to delineate gene regulatory elements from bulk chromatin by recruiting factors that create unique chromatin architecture. This study provides information about binding of lysine demethylase enzyme KDM2A in mouse embryonic stem cells.

2010-04-27 | E-GEOD-18588 | biostudies-arrayexpress

Lysine-specific demethylase 1 metastasis of androgen-independent PCa cells

Project description:Lysine-specific demethylase 1 metastasis of androgen-independent PCa cells

| PRJNA245395 | ENA