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Doxorubicin induces double-strand breaks at CpG island promoters

ABSTRACT: Doxorubicin induces double-strand breaks at CpG island promoters

PROVIDER: PRJNA266225 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR1638870.fastq.gz	Fastqsanger.gz
	SRR1638880.fastq.gz	Fastqsanger.gz
	SRR1638871.fastq.gz	Fastqsanger.gz
	SRR1638881.fastq.gz	Fastqsanger.gz
	SRR1638872.fastq.gz	Fastqsanger.gz

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Doxorubicin induces double-strand breaks at CpG island promoters

Project description:Doxorubicin is a widely used chemotherapeutic drug that intercalates between DNA base-pairs and posions Topoisomerase II, although the mechanistic basis for cell killing remains speculative. Here we show that both anthracyclines and Topoisomerase II poison cause enhanced DNA double-strand breaks around CpG island promoters of active genes genome-wide. We propose that torsion-based enhancement of nucleosome turnover exposes promoter DNA, ultimately causing DNA breaks around promoters that contributes to cell killing. We have analyzed mouse squamous cell carcinoma cells treated with doxorubicin, aclarubicin and etoposide. The direct in situ Breaks Labeling, Enrichment on Streptavidin (BLESS, PMID 23503052) method was used for mapping DNA double-strand breaks genome-wide.

2015-01-31 | E-GEOD-62927 | biostudies-arrayexpress

Doxorubicin induces double-strand breaks at CpG island promoters

2015-01-31 | GSE62927 | GEO

Doxorubicin induces double-strand breaks at CpG island promoters

Project description:Doxorubicin induces double-strand breaks at CpG island promoters

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Project description:The anthracycline doxorubicin is a highly effective anti-cancer drug associated with severe side effects, including secondary tumors and cardiotoxicity. Doxorubicin induces DNA damage through double-strand breaks (DSBs) and epigenetic or chromatin damage through histone eviction. We examined whether separation of these activities can help to detoxify doxorubicin, while maintaining its chemotherapeutic efficacy. We show that anthracycline variants harboring the histone eviction activity alone remain potent anti-cancer drugs, while greatly alleviating cardiotoxicity and secondary tumor formation. We thus demonstrate that treatment-limited side effects of doxorubicin can be synthesized away, yielding effective chemotherapeutics towards improved and prolonged treatment responses and higher patient quality of life.

2019-09-01 | GSE108179 | GEO

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DNA double-strand breaks induced by high NaCl occur predominantly in gene deserts

Project description:High concentration of NaCl increases DNA breaks both in cell culture and in vivo. The breaks remain elevated as long as NaCl concentration remains high and are rapidly repaired when the concentration is lowered. Repair of the breaks after NaCl is reduced is accompanied by formation of foci containing phosphorylated H2AX (γH2AX), which occurs around DNA double-strand breaks and contributes to their repair. By chromatin immunoprecipitation using anti-γH2AX antibody, followed by massive parallel sequencing (ChIP-Seq), we find that during repair of double–strand breaks induced by high NaCl, γH2AX is predominantly localized to regions of the genome devoid of genes (“gene deserts”), indicating that the high NaCl-induced double-strand breaks are located there. Localization to gene deserts helps explain why the DNA breaks are less harmful than are the random breaks induced by genotoxic agents such as UV radiation, ionizing radiation and oxidants. We propose that the universal presence of NaCl around animal cells has directly influenced the evolution of the structure of their genomes.

2011-11-21 | GSE32882 | GEO

DNA double-strand breaks induced by high NaCl occur predominantly in gene deserts

Project description:High concentration of NaCl increases DNA breaks both in cell culture and in vivo. The breaks remain elevated as long as NaCl concentration remains high and are rapidly repaired when the concentration is lowered. Repair of the breaks after NaCl is reduced is accompanied by formation of foci containing phosphorylated H2AX (M-NM-3H2AX), which occurs around DNA double-strand breaks and contributes to their repair. By chromatin immunoprecipitation using anti-M-NM-3H2AX antibody, followed by massive parallel sequencing (ChIP-Seq), we find that during repair of doubleM-bM-^@M-^Sstrand breaks induced by high NaCl, M-NM-3H2AX is predominantly localized to regions of the genome devoid of genes (M-bM-^@M-^\gene desertsM-bM-^@M-^]), indicating that the high NaCl-induced double-strand breaks are located there. Localization to gene deserts helps explain why the DNA breaks are less harmful than are the random breaks induced by genotoxic agents such as UV radiation, ionizing radiation and oxidants. We propose that the universal presence of NaCl around animal cells has directly influenced the evolution of the structure of their genomes. ChIP-Seq experiment to find locations of M-NM-3H2AX in mouse genome

2011-11-21 | E-GEOD-32882 | biostudies-arrayexpress

Epigenetic changes due to histone eviction induced by anthracycline doxorubicin and aclarubicin

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2013-06-04 | E-GEOD-33633 | biostudies-arrayexpress

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