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Doxorubicin Changes the Spatial Organization of the Genome around Active Promoters

ABSTRACT: To investigate the function of TOP2 on chromatin structure of human cells, we performed Hi-C using chromatin obtained from RPE1 cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE214912 | GEO | 2023/03/31

REPOSITORIES: GEO

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Doxorubicin Changes the Spatial Organization of the Genome around Active Promoters

Project description:To investigate the function of the TOP2 inhibitors treatment in binding of chromatin architecture factors, we performed ChIP-seq. We used chromatin from RPE1 cells treated with four different conditions: control (DMSO-treatment), doxorubicin treatment (200 nM and 340 nM) and ICRF193 treatment (5uM).

2023-03-31 | GSE215318 | GEO

Doxorubicin Changes the Spatial Organization of the Genome around Active Promoters

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

2023-03-31 | GSE215325 | GEO

Doxorubicin Changes the Spatial Organization of the Genome around Active Promoters

Project description:To investigate the function of the doxorubicin treatment in differentiation expression of human genes, we performed gene expression profiling analysis using data obtained from RNA-seq of three different conditions: control (DMSO-treatment) and doxorubicin treatment (200 nM and 340 nM).

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Doxorubicin enhances nucleosome turnover around promoters

Project description:We use a metabolic labeling strategy for directly measuring nucleosome turnover to examine the effect of doxorubicin on chromatin dynamics in squamous cell carcinoma cell lines derived from genetically defined mice. We find that doxorubicin enhances nucleosome turnover around gene promoters, and turnover correlates with gene expression level. Keywords: Chromatin affinity-purification on microarray 26 CATCH-IT arrays and 8 expression arrays.

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Doxorubicin enhances nucleosome turnover around promoters

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Doxorubicin enhances nucleosome turnover around promoters.

Project description:Doxorubicin is an anthracycline DNA intercalator that is among the most commonly used anticancer drugs. Doxorubicin causes DNA double-strand breaks in rapidly dividing cells, although whether it also affects general chromatin properties is unknown. Here, we use a metabolic labeling strategy to directly measure nucleosome turnover to examine the effect of doxorubicin on chromatin dynamics in squamous cell carcinoma cell lines derived from genetically defined mice. We find that doxorubicin enhances nucleosome turnover around gene promoters and that turnover correlates with gene expression level. Consistent with a direct action of doxorubicin, enhancement of nucleosome turnover around promoters gradually increases with time of exposure to the drug. Interestingly, enhancement occurs both in wild-type cells and in cells lacking either the p53 tumor suppressor gene or the master regulator of the DNA damage response, ATM, suggesting that doxorubicin action on nucleosome dynamics is independent of the DNA damage checkpoint. In addition, another anthracycline drug, aclarubicin, shows similar effects on enhancing nucleosome turnover around promoters. Our results suggest that anthracycline intercalation promotes nucleosome turnover around promoters by its effect on DNA topology, with possible implications for mechanisms of cell killing during cancer chemotherapy.

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Spatial chromosome folding and active transcription drive DNA fragility and formation of oncogenic MLL translocations [RNA-Seq]

Project description:How spatial chromosome organization influences genome integrity is still poorly understood. Here we show that DNA double-strand breaks (DSBs) mediated by topoisomerase 2 (TOP2) activities, are enriched at chromatin loop anchors with high transcriptional activity. Recurrent DSBs occur at CTCF/cohesin bound sites at the bases of chromatin loops and their frequency positively correlates with transcriptional output and directionality. The physiological relevance of this preferential positioning is indicated by the finding that genes recurrently translocating to drive leukemias, are highly transcribed and are enriched at loop anchors. These genes accumulate DSBs at recurrent hot spots that give rise to chromosomal fusions relying on the activity of both TOP2 isoforms and on transcriptional elongation. We propose that transcription and 3D chromosome folding jointly pose a threat to genomic stability, and are key contributors to the occurrence of genome rearrangements that drive cancer.

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