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Suppression of poised oncogenes by ZMYND8 promotes chemo-sensitization

ABSTRACT: In this study, we have shown how ZMYND8, a putative chromatin reader, chemosensitizes, chemo-resistant breast cancer cells, by modulating poised oncogenes.

ORGANISM(S): Homo sapiens

PROVIDER: GSE145141 | GEO | 2021/01/01

REPOSITORIES: GEO

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Suppression of poised oncogenes by ZMYND8 promotes chemo-sensitization

Project description:Suppression of poised oncogenes by ZMYND8 promotes chemo-sensitization

| PRJNA606181 | ENA

Suppression of poised oncogenes by ZMYND8 promotes chemo-sensitization

Project description: Not available

| S-EPMC7738522 | biostudies-literature

Microarray upon ZMYND8 knockdown in Hela cells

Project description:ZMYND8, a chromatin reader/effector protein, knockdown in Hela cells

2018-11-09 | GSE106900 | GEO

Microarray upon ZMYND8 knockdown in MCF7 cells

Project description:ZMYND8, a chromatin reader/effector protein, knockdown in MCF7 cells

2018-11-09 | GSE106723 | GEO

ZMYND8 Suppresses MAPT213 LncRNA Transcription To Promote Neuronal Differentiation

Project description:In this study, we have shown how ZMYND8, a putative chromatin reader, role in neuronal differentiation.

2022-09-16 | GSE196029 | 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

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

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

Multivalent histone and DNA engagement by the triple reader module of ZMYND8 directs the recruitment of a transcriptional network to genes to regulate gene expression

Project description:Elucidation of multivalent interactions involving both DNA and histone post-translational-modifications (PTMs) is essential for providing insight into complex biological functions. We report here the high resolution crystal structure of the N-terminal triple reader module (PHD-Bromo-PWWP) of ZMYND8, which forms a stable unit, capable of simultaneously recognizing histone PTMs and providing a charged platform for DNA interaction. Monte Carlo simulations provide a model whereby the reader module directly engages the core nucleosome particle, extracting the entire histone H3 tail and initiating contacts with the DNA super-coil structure. Systematic mutation of these interaction interfaces reveals cooperativity within the ensemble. Single domain disruption destroys the functional network of interactions initiated by ZMYND8, which impairs recruitment to sites of DNA damage and alters transcription. Taken together, our results establish an important role of the ZMYND8 multivalent reader module in nucleosome binding and chromatin function.

2021-04-30 | GSE75624 | GEO

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