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Anti-cancer drugs curaxins target the 3D genome organization [ChIP-seq]

ABSTRACT: Anti-cancer drugs curaxins target the 3D genome organization [ChIP-seq]

PROVIDER: PRJNA505308 | ENA |

REPOSITORIES: ENA

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Anti-cancer drugs curaxins target the 3D genome organization

Project description:Anti-cancer drugs curaxins target the 3D genome organization

| PRJNA505307 | ENA

Anti-cancer drugs curaxins target the 3D genome organization [HiC]

Project description:Anti-cancer drugs curaxins target the 3D genome organization [HiC]

| PRJNA482566 | ENA

Anti-cancer drugs curaxins target the 3D genome organization [HiC]

Project description:We have recently discovered a class of anti-cancer agents, curaxins, which suppress transcription of oncogenes. Here we demonstrate that curaxins preferentially downregulate expression of genes controlled by enhancers and super-enhancers via interrupting enhancer/promoter spatial communication. Our observations made both on a model of enhancer-regulated transcription of chromatinized template and on cultured cancer cells allow classifying curaxins as a novel type of epigenetic drugs that target the 3D genome organization.

2019-02-18 | GSE117582 | GEO

Anti-cancer drugs curaxins target the 3D genome organization [ChIP-seq]

2019-02-18 | GSE122462 | GEO

Chemical profiling of the genome with anti-cancer drugs defines target specificities

Project description:Many anti-cancer drugs induce DNA breaks to eliminate tumor cells. The anthracycline topoisomerase II inhibitors can also evict histones. We performed a genome-wide high-resolution mapping of chemotherapeutic effects of various topoisomerase I and II inhibitors. We show that different drugs target different types of chromatin for induction of DNA damage and histone eviction. Topoisomerase inhibitors topotecan and etoposide similarly target transcriptionally active chromatin for DNA damage. Daunorubicin induces DNA breaks and evicts histones in active chromatin, thus quenching local DNA damage response. The analog aclarubicin evicts histones in H3K27me3-marked heterochromatin. These results can guide rational treatment decisions regarding these genome manipulating anti-cancer drugs. FAIRE-seq and g-H2AX ChIP-seq were performed on K562 cells after drug exposure

2015-05-10 | E-GEOD-60395 | biostudies-arrayexpress

Chemical profiling of the genome with anti-cancer drugs defines target specificities

2015-05-10 | GSE60395 | GEO

Anti-cancer drugs curaxins target the 3D genome organization

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

2019-02-18 | GSE122463 | GEO

Cohesin Regulates 3D Accessible Genome Organization and Function

Project description:we combined Assay for Transposase-Accessible Chromatin and lattice light-sheet PALM microscopy (3D ATAC-PALM) to selectively image key features of the 3D accessible genome in single cells. We found that accessible chromatin domains (ACDs) form spatially segregated clusters in the nucleus. Rapid depletion of CTCF or Cohesin (RAD21 subunit) induced extensive 3D spatial mixing of ACD clusters and reduced physical separation between ACDs within chromosomes. Experimental perturbations and modeling suggest that both weak, multivalent, dynamic protein-protein interactions together with loop extrusion influence ACD organization. Live-cell studies suggest that ACD clustering regulates transcription factor binding site distribution, target search kinetics and binding dynamics. Here we report the ATAC-seq results from Tn5 PA549 and nextera Tn5 upon various chemical and genetic perturbations.

2022-02-01 | GSE144505 | GEO

Cohesin Regulates 3D Accessible Genome Organization and Function

Project description:Cohesin Regulates 3D Accessible Genome Organization and Function

| PRJNA603822 | ENA

The anti-cancer drugs curaxins target spatial genome organization.

Project description:Recently we characterized a class of anti-cancer agents (curaxins) that disturbs DNA/histone interactions within nucleosomes. Here, using a combination of genomic and in vitro approaches, we demonstrate that curaxins strongly affect spatial genome organization and compromise enhancer-promoter communication, which is necessary for the expression of several oncogenes, including MYC. We further show that curaxins selectively inhibit enhancer-regulated transcription of chromatinized templates in cell-free conditions. Genomic studies also suggest that curaxins induce partial depletion of CTCF from its binding sites, which contributes to the observed changes in genome topology. Thus, curaxins can be classified as epigenetic drugs that target the 3D genome organization.

| S-EPMC6441033 | biostudies-literature

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