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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Expression data from QdNOs treated Escherichia coli

ABSTRACT: Cyadox(CYA), as a new species of Quinoxaline 1, 4-dioxides and olaquindox(OLA) both showed higher antibacterial activity under anaerobic incubation. Microarray was used for global gene expression studies, which were further confirmed by real-time PCR. Cyadox and olaquindox mainly stimulated the expression of DNA repair genes as a response to the DNA damage. The induced gene sbmC was found to provide partial protection against the antibiotics of gyrase inhibitors like the quinolones and the ruvAB helped remove the topoisomerase IV-DNA cleavage complex caused by some type IIA topoisomerase poison antibiotics. It was inferred that the radical intermediate of cyadox reduction under anaerobic condition was responsible for the poison effect of IIA topoisomerases, which brought about DNA double stand breaks and other DNA damages in E. coli. We applied subinhibitory concentrations (concentrations that cause little growth inhibition) of two drus with the goal of observing antibiotic-specific primary expression profiles, and higher concentrations of drugs had been shown to cause a broader effect on cellular processes, thereby giving more complex response patterns and dose-specific effects could be examined.To the end, drugs were added to a final concentration of 0.5MIC(2) and MBC(3) for cyadox, and MIC(4) and MBC(5) for olaquindox, respectively. Control with 1% (vol/vol) DMSO(1) was grown in parallel.

ORGANISM(S): Escherichia coli

SUBMITTER: li bei

PROVIDER: E-GEOD-39607 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Expression data from QdNOs treated Escherichia coli

Project description:Cyadox(CYA), as a new species of Quinoxaline 1, 4-dioxides and olaquindox(OLA) both showed higher antibacterial activity under anaerobic incubation. Microarray was used for global gene expression studies, which were further confirmed by real-time PCR. Cyadox and olaquindox mainly stimulated the expression of DNA repair genes as a response to the DNA damage. The induced gene sbmC was found to provide partial protection against the antibiotics of gyrase inhibitors like the quinolones and the ruvAB helped remove the topoisomerase IV-DNA cleavage complex caused by some type IIA topoisomerase poison antibiotics. It was inferred that the radical intermediate of cyadox reduction under anaerobic condition was responsible for the poison effect of IIA topoisomerases, which brought about DNA double stand breaks and other DNA damages in E. coli.

2012-07-25 | GSE39607 | GEO

Topoisomerase II inhibition involves characteristic chromosomal expression patterns: Doxorubicin study

2008-10-01 | GSE11940 | GEO

Transcription profiling by array of human hepatocytes treated with doxorubicin

Project description:A variety of important anticancer drugs kill cells by increasing cellular levels of topoisomerase II-DNA cleavage complex. The anthracycline anticancer drug doxorubicin forms a stable ternary complex with DNA and topoisomerase IIa, thereby inhibiting the normal function of the enzyme. In this study we found genes regulated by doxorubicin - induced and repressed - to be located much closer to each other than genes distributed randomly all over the genome (< 100 kbp). Experiment Overall Design: We calculated specifically the probability by which particular genes which were deregulated by the treatment of human hepatocytes with doxorubicin will occur within DNA windows of different sizes as compared to the probability of all known mapped genes (RefSeq transcripts) of the human genome (NCBI RefSeq 19,360; build 36.2) to occur within the same DNA windows.

2008-10-10 | E-GEOD-11940 | biostudies-arrayexpress

Doxorubicin induces double-strand breaks at CpG island promoters

2015-01-31 | GSE62927 | GEO

Topoisomerase I Poisoning by Electrophiles Derived from Oxidative Stress

Project description:The cancer target enyzme topoisomerase 1 transiently cleaves one strand of chromosomal DNA to relax accumulated strain that can prevent transcription, replication or chromatin assembly. The topoisomerase 1 poison camptothecin and its synthetic analogs are widely used chemotherapeutics that act by trapping the enzyme on DNA in a ‘covalent complex’, resulting in persistent DNA damage and cell death. The prevailing model, interfacial inhibition, contends that the covalent complex is trapped by drug binding alone. In contrast, here we show that camptothecins produce extensive oxidative stress and that topoisomerase 1 is reactive with electrophilic second messengers of oxidative damage. We show that blocking oxidative stress in cells inhibits covalent complex formation by camptothecin, while electrophiles such as 4-hydroxynonenal are able to induce covalent complex formation in cells on their own. Towards mechanism of action, we show that 4-hydroxynonenal electrophilically modifies a cysteine within the DNA-binding active site of human topoisomerase 1. Taken together, our results suggest a mechanism in which oxidative stress mediates the effects of many topoisomerase 1 poisons, and suggest that this critical DNA-regulating enzyme may have a dual role as a sensor of cellular redox stress, linking oxidative stress to DNA damage response in cancer cells.

2021-03-24 | PXD018549 | Pride

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

Transcription profiling by array of Burkholderia cenocepacia J2315 wild type and antibiotic-resistant mutants exposed to sub-inhibitory concentrations of drugs

Project description:Burkholderia cenocepacia J2315 wild type and adaptive mutants with elevated resistance to antibiotics were exposed to sub-inhibitory concentrations of drugs

2010-08-01 | E-MEXP-2738 | biostudies-arrayexpress

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

Sublethal concentrations of antibiotics cause shift to anaerobic metabolism in Listeria monocytogenes and induce phenotypes linked to antibiotic tolerance

Project description:The human pathogenic bacterium Listeria monocytogenes was exposed to antibiotics both during clinical treatment and as a saprophyte. As one of the keys to successful treatment is continued antibiotic sensitivity, the purpose of this study was to determine if exposure to sublethal antibiotic concentrations would affect the bacterial physiology and potentially induce tolerance to antibiotics. Transcriptomic analyses demonstrated that each of four antibiotics caused a compound-specific gene expression pattern related to (the) mode-of-action of the particular antibiotic. All four antibiotics caused the same changes in expression of several metabolic genes indicating a shift from aerobic to anaerobic metabolism driven by the induction of lmo1634 and the repression of alsA and lmo1992. This shift in metabolism could be a survival strategy in response to antibiotics and is further supported by the observation that a Δlmo1634 mutant was more sensitive to bactericidal antibiotics. The monocin locus encoding a cryptic prophage was induced by co-trimoxazole and repressed by ampicillin and gentamicin. This expression pattern correlated with the observed antibiotic-dependent biofilm formation, indicating a role of monocin in antibiotic-induced biofilm formation and a ΔlmaDCBA mutant confirmed this correlation. Thus, sublethal concentrations of antibiotics caused metabolic and physiological changes indicating that the organism is preparing to withstand lethal concentrations of antibiotics.

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