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ZMYND8 is a negative regulator of ferroptosis in BCSCs

ABSTRACT: ZMYND8 is a negative regulator of ferroptosis in BCSCs

PROVIDER: PRJNA941858 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23719913.fastq.gz	Fastqsanger.gz
	SRR23719914.fastq.gz	Fastqsanger.gz
	SRR23719915.fastq.gz	Fastqsanger.gz
	SRR23719916.fastq.gz	Fastqsanger.gz

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ZMYND8 is a negative regulator of ferroptosis in BCSCs

Project description:ZMYND8 Protects Breast Cancer Stem Cells against Oxidative Stress and Ferroptosis through Activation of NRF2

2024-02-19 | GSE226834 | GEO

Regulation of 27-hydroxycholesterol metabolism by ZMYND8

Project description:ZMYND8 is a master regulator of 27-hydroxycholesterol metabolism in breast cancer stem cells.

2022-06-02 | GSE186543 | GEO

ZMYND8 reads the dual histone mark H3K4me1-H3K14ac to antagonize the expression of metastasis-linked genes

Project description:Histone acetylation, including acetylated H3K14 (H3K14ac), is generally linked to gene activation. Monomethylated histone H3 lysine 4 (H3K4me1), together with other gene-activating marks, denotes active genes. In contrast to usual gene-activating functions of H3K14ac and H3K4me1, we here show that the dual histone modification mark H3K4me1-H3K14ac is recognized by ZMYND8 (also called RACK7) and functions to counteract gene expression. We identified ZMYND8 as a transcriptional corepressor of the H3K4 demethylase JARID1D. ZMYND8 antagonizes the expression of metastasis-linked genes, and its knockdown increases the cellular invasiveness in vitro and in vivo. The plant homeodomain (PHD) and Bromodomain cassette in ZMYND8 mediates the combinatorial recognition of H3K4me1-H3K14ac and H3K4me0-H3K14ac by ZMYND8. These findings uncover an unexpected role for the signature H3K4me1-H3K14ac in attenuating gene expression and reveal a previously unknown metastasis-suppressive epigenetic mechanism in which ZMYND8's PHD-Bromo cassette couples H3K4me1-H3K14ac with repression of metastasis-linked genes. i) ChIP-Seq data of ZMYND8, JARID1D, H3K4me1, H3K14ac, H3K4me3, and H3K27me3 in normal DU145 cells. ii) ChIP-Seq data of H3K4me1 and H3K4me3 in shLuciferase-, shJARID1D-, or shZMYND8-treated DU145 cells. iii) RNA-Seq data in shLuciferase-, shJARID1D-, or shZMYND8-treated DU145 cells.

2016-07-28 | E-GEOD-82260 | biostudies-arrayexpress

Regulation of 27-hydroxycholesterol metabolism by ZMYND8 in mammospheres

Project description:ZMYND8 is a master regulator of 27-hydroxycholesterol metabolism in breast cancer stem cells.

2022-06-02 | GSE203054 | GEO

All the regulated lncRNAs and mRNAs in BCSCs derived exosomes compared to non-BCSCs derived exosomes

Project description:Transcriptional landscapes between exosomes derived from BCSCs and non-BCSCs were compared using the LC Human ceRNA array V1.0 (4*180K, Design ID:085202) Microarray. Goal was to investigate potential lncRNAs involved in breast cancer progression through enveloping into exosomes.

2024-01-31 | GSE254074 | GEO

Gene expression change after targeted degradation of ZMYND8 or IRF8

Project description:Cancer cell type-selective addiction of transcription-chromatin regulatory program provides opportunities for therapeutic interventions. Here, we uncovered an IRF8-MEF2D transcription factor (TF) regulatory circuit as an acute myeloid leukemia (AML)-biased dependency. Combining CRISPR-based genetic screens, transcriptional analysis, and chromatin profiling, we demonstrated that a chromatin regulator, ZMYND8, directly regulates IRF8 and MYC expression through occupying AML-specific enhancer regions. ZMYND8 was essential for AML proliferation both in vitro and in vivo. The ZMYND8-occupied IRF8 enhancer was further characterized using Circular Chromosome Conformation Capture and CRISPRi-based perturbation assays and was observed in primary patient cells. Importantly, mutagenesis experiments revealed that the PHD/Bromodomain/PWWP reader module is required for ZMYND8 tethering to leukemia-essential co-activator BRD4 for enhancer-mediated gene regulation. Our results rationalize ZMYND8 as a potential selective therapeutic target for modulating the IRF8/MYC transcriptional networks in AML.

2021-09-06 | GSE157633 | GEO

Gene expression change after inactivation of ZMYND8 by CRISPR-Cas9

2021-09-06 | GSE157632 | GEO

All the regulated lncRNAs in breast cancer stem cells (BCSCs, CD44+CD24- sorted)MCF-7 cells compared to non-BCSCs (non-CD44+CD24- sorted) MCF-7 cells

Project description:Circulating transcriptional landscapes between BCSCs and non-BCSCs were compared using the Affymetrix Human OE LncRNA Microarray with probes for profiling of 63542 human lncRNAs. Goal was to investigate potential lncRNAs involved in BCSCs progression.

2019-01-26 | GSE125678 | GEO

Transcriptome profiling of control and Zmynd8-cKO mouse cardiomyocyte

Project description:Appropriate gene expression within cardiomyocytes is coordinated by chromatin factors and is essential for heart function. We investigated the role of the chromatin reader ZMYND8 in the mouse heart using null and conditional knockouts (Zmynd8-cKO). While full-length Zmynd8 is not required for cardiomyocyte development, Zmynd8-cKO mice develop cardiomegaly, decreased cardiac function, and premature death compared to controls. Transcriptome analysis of Zmynd8-cKO cardiomyocytes reveals illegitimate expression of transcripts and proteins normally limited to skeletal muscle and integration of TNNI2 skeletal troponin into cardiac sarcomeres of mutant mice. We conclude that ZMYND8 is necessary to maintain appropriate cardiomyocyte homeostasis and gene expression.

2022-10-24 | GSE216254 | GEO

The Chromatin Reader ZMYND8 Regulates Igh Enhancers to Promote Immunoglobulin Class Switch Recombination

Project description:Class Switch Recombination (CSR) is a DNA recombination reaction that diversifies the effector component of antibody responses. CSR is initiated by activation-induced cytidine deaminase (AID), which targets transcriptionally active immunoglobulin heavy chain (Igh) switch donor and acceptor DNA. The 3’ Igh super-enhancer, 3’ Regulatory Region (3’RR), is essential for acceptor region transcription, but how this function is regulated is unknown. Here we identify the chromatin reader ZMYND8 as an essential regulator of the 3’RR and CSR. In B cells, ZMYND8 binds promoters and super-enhancers, including the 3’RR, and controls its activity by modulating the enhancer transcriptional status. In its absence, there is increased 3’RR polymerase loading, and decreased acceptor region transcription and CSR. In addition to CSR, ZMYND8 deficiency impairs somatic hypermutation (SHM) of Igh, which is also dependent on the 3’RR. Thus ZMYND8 controls Igh diversification in mature B lymphocytes by regulating the activity of the 3’ Igh super-enhancer.

2018-10-04 | GSE118794 | GEO

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