E-GEOD-11940
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: PRJNA109251PRJNA109253PRJNA105795
PROVIDER: E-GEOD-11940 | ExpressionAtlas | 2015-08-27
REPOSITORIES: ExpressionAtlas
Similar Datasets
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). Keywords: Doxorubicin-treated human hepatocytes versus non-treated human hepatocytes
2008-10-01 | GSE11940 | GEO
Project description:This SuperSeries is composed of the following subset Series:; GSE11940: Topoisomerase II inhibition involves characteristic chromosomal expression patterns: Doxorubicin study; GSE11941: Topoisomerase II inhibition involves characteristic chromosomal expression patterns: Trovafloxacin study Experiment Overall Design: Refer to individual Series
2008-10-26 | E-GEOD-11942 | biostudies-arrayexpress
Project description:We have used chromatin immune-precipitation with parallel sequencing (ChIP-Seq) technology to identify genome-wide H3K4me3 binding in human lymphoblastoid cell lines treated with a DNA-damaging chemotherapeutic reagent doxorubicin. ChIP-Seq analysis of H3K4me3 binding sites in human lymphoblastoid cells treated with Doxorubicin or vehicle
2014-11-14 | E-GEOD-51713 | biostudies-arrayexpress
Project description:We have used chromatin immune-precipitation with parallel sequencing (ChIP-Seq) technology to identify genome-wide p53 binding in human lymphoblastoid cell lines treated with a DNA-damaging chemotherapeutic reagent doxorubicin. ChIP-Seq analysis of p53 binding sites in human lymphoblastoid cells treated with Doxorubicin or vehicle
2013-10-23 | E-GEOD-46991 | biostudies-arrayexpress
Project description:In order to determine molecular rules for transcriptional regulation of targeted genes to explain in part the pleiotropic effect observed in animals and humans upon exposure to Aroclor 1254 we treated human hepatocytes with Aroclor1254 and analysed RNA expression using a Nimblegene human custom array. Keywords: Human hepatocytes, Aroclor1254 treatment, 20µM, 72h
2006-08-01 | GSE5213 | GEO
Project description:Primary human hepatocytes were treated with compounds modulating steatosis: palmitic acid, compound C and metformin qPCR miRNA expression profiling. Hepatocytes were treated as indicated in the summary. Equal amount total RNA was pooled prior to miRNA expression analysis
2020-02-11 | GSE145039 | GEO
Project description:The incidence of obesity and its related morbidities has rapidly increased over the past twenty years. One consequence of this is the increased probability of having to treat obese individuals for breast cancer. An important co-morbidity associated with obesity are the spectrum of fatty liver diseases. As such, an important question is how treatment of breast cancer with standard therapeutic agents may alter in individuals with fatty liver disease. Such impacts could result in an enhanced adverse effect profile over both acute (e.g. increased cytotoxicity against non-malignant tissues) or chronic (e.g. increased progression through the fatty liver disease spectrum) time periods. In this work we examine if lipid loading in human hepatocytes, leading to a steatotic phenotype, results in an altered toxic liability for the cancer therapeutic doxorubicin. We demonstrate that there is a synergistic impact on cytotoxicity, due to increased oxidative stress. Array analysis reveals the cellular changes associated with hepatocyte adaptation to lipid loading or doxorubicin treatment alone, and how these profiles are significantly altered during doxorubicin treatment of lipid-loaded hepatocytes. Such alterations, we believe, not only underlie the enhanced sensitivity of obese individuals to the acute adverse effects of doxorubicin, but may also potentiate transition along the fatty liver disease spectrum.Experimental design: Huh7 cells were exposed to lipid and/or doxorubicin as required. Huh7 cells were treated with vehicle control or 300 μM FFA mixture for 24 h in T25 culture flasks. The following day, the cells were treated with either 300 μM FFA mixture, 0.1 μM or 3.6 μM DOX and incubated for 4 hrs or 12 hrs. By the end of incubation time, Total RNA was extracted from cells using the RNeasy Plus Mini Kit (QIAGEN-UK) according to the instructions of manufacturer. RNA samples were sent to the Central Biotechnology Services (Cardiff University, UK), for quality control, synthesis of biotin-labeled cRNA, and hybridisation against Illumina Human-HT12 (Illumina, Inc., Hayward, CA) chips. Washed chips were scanned with Bead Station 500x (Illumina) and the signal intensities quantified with BeadStudio (Illumina). To ensure high quality results from the microarray data, RNA samples were extracted from three independent treatments, giving a biological n = 3 per treatment which gives statistical power to increase the confidence of the results/conclusions generated from the microarray experiment.
2015-06-01 | E-MTAB-3523 | biostudies-arrayexpress
Project description:To gain into the molecular mechanisms and pathways involved in doxorubicin induced cardiotoxicity, we performed whole genome transcriptome profiling via RNA-seq in hESCs-derived CMs treated with doxorubicin or vehicle only control. Cells were treated with 0, 1 or 2.5 μM of doxorubicin for 16 hours and RNA was isolated for high throughput sequencing
2018-02-21 | GSE106297 | GEO
Project description:Primary human hepatocytes treated with IFNalpha and IL28B
| PRJNA144839 | ENA
Project description:NF-kB has been linked to doxorubicin-based chemotherapy resistance in breast cancer patients. NF-kB nuclear translocation and DNA binding in doxorubicin treated-breast cancer cells have been extensively examined, however its functional consequences in terms the spectrum of NF-kB -dependent genes expressed and, thus, the impact on tumour cell behaviour are unclear. We hypothesized that NF-kB gene expression profile induced by doxorubicin might be different among breast cancer cells and tumors. Doxorubicin treatment in the p53-mutated MDA-MB-231 cells resulted in NF-kB driven-gene transcription demonstrated by gene expression microarrays. Selected genes (ICAM-1, CXCL1, IL8) related with invasion, metastasis and chemoresistance expression were confirmed by RT-PCR in a subset of additional doxorubicin-treated cells and fresh primary human breast tumors. In both systems, p53-deficient background correlated with the activation of these NF-kB targeted genes. Overexpression of p53WT in the mutant p53 MDA-MB-231 cells impaired NF-kB driven transcription induced by doxorubicin. Moreover, tumors with a p53 deficient background and nuclear NF-kB /p65 expression correlated with reduced disease free-survival. This study supports that tumor molecular profiles for doxorubicin driven NF-kB-response are likely to exist. A link between p53 deficiency and the presence of active transcriptionally NF-kB could favour an aggressive behaviour and might have implications for doxorubicin-based chemotherapy in breast tumors exhibiting aberrant p53 activity 12 samples were analyzed: controls (n=3); Doxorubicin treated (n=3); MLN120B treated (n=3); MLN120B + Doxorubicin treated (n=3)
2013-12-31 | E-GEOD-47013 | biostudies-arrayexpress