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Expression data from 5 human cell lines exposed to IR (5 Gy)

ABSTRACT: The cellular response to DNA damage is vital for maintaining genomic stability and preventing undue cell death or cancer formation. The DNA damage response (DDR), most robustly mobilized by double-strand breaks (DSBs), rapidly activates an extensive signaling network that affects numerous cellular systems, leading to cell survival or programmed cell death. A major component of the DDR is the widespread modulation of gene expression. We analyzed transcriptional responses to ionizing radiation (IR) in 5 human cell lines to elucidate the scope of this response and identify its gene targets. According to the mRNA expression profiles most of the responses were cell line-specific. Data analysis identified significant enrichment for p53 target genes and cell cycle-related pathways among groups of up-regulated and down-regulated genes, respectively.

ORGANISM(S): Homo sapiens

PROVIDER: GSE30240 | GEO | 2011/08/01

SECONDARY ACCESSION(S): PRJNA143767

REPOSITORIES: GEO

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Expression data from 5 human cell lines exposed to IR (5 Gy)

Project description:The cellular response to DNA damage is vital for maintaining genomic stability and preventing undue cell death or cancer formation. The DNA damage response (DDR), most robustly mobilized by double-strand breaks (DSBs), rapidly activates an extensive signaling network that affects numerous cellular systems, leading to cell survival or programmed cell death. A major component of the DDR is the widespread modulation of gene expression. We analyzed transcriptional responses to ionizing radiation (IR) in 5 human cell lines to elucidate the scope of this response and identify its gene targets. According to the mRNA expression profiles most of the responses were cell line-specific. Data analysis identified significant enrichment for p53 target genes and cell cycle-related pathways among groups of up-regulated and down-regulated genes, respectively. Expression profiles were measured using affymetrix chips in IR- irradiated G361 cells and their time-matched untreated controls. Time points recorded were 0, 3 and 6 hrs. IR dose: 5 Gy Expression profiles were measured using affymetrix chips in IR- irradiated HepG2 cells and their time-matched untreated controls. Time points recorded were 0, 3 and 6 hrs. IR dose: 5 Gy Expression profiles were measured using affymetrix chips in IR- irradiated TK6 cells and their time-matched untreated controls. Time points recorded were 0, 3 and 6 hrs. IR dose: 5 Gy Expression profiles were measured using affymetrix chips in IR- irradiated U2OS cells and their time-matched untreated controls. Time points recorded were 0, 3 and 6 hrs. IR dose: 5 Gy Expression profiles were measured using affymetrix chips in IR- irradiated BJ cells and their time-matched untreated controls. Time points recorded were 0, 3 and 6 hrs. IR dose: 5 Gy

2011-07-31 | E-GEOD-30240 | biostudies-arrayexpress

Nuclear poly(A)-binding protein 1 is an ATM target and essential for DNA double-strand break rep

Project description:The DNA damage response (DDR) is an extensive signaling network that is robustly mobilized by DNA double-strand breaks (DSBs). The primary transducer of the DSB response is the protein kinase, ataxia-telangiectasia, mutated (ATM). Here, we establish nuclear poly(A)-binding protein 1 (PABPN1) as a novel target of ATM and a crucial player in the DSB response. PABPN1 usually functions in regulation of RNA processing and stability. We establish that PABPN1 is recruited to the DDR as a critical regulator of DSB repair. A portion of PABPN1 relocalizes to DSB sites and is phosphorylated on Ser95 in an ATM-dependent manner. PABPN1 depletion sensitizes cells to DSBinducing agents and prolongs the DSB-induced G2/M cell-cycle arrest, and DSB repair is hampered by PABPN1 depletion or elimination of its phosphorylation site. PABPN1 is required for optimal DSB repair via both nonhomologous end-joining (NHEJ) and homologous recombination repair (HRR), and specifically is essential for efficient DNAend resection, an initial, key step in HRR. Using mass spectrometry analysis, we capture DNA damage-induced interactions of phospho-PABPN1, including well-established DDR players as well as other RNA metabolizing proteins. Our results uncover a novel ATM-dependent axis in the rapidly growing interface between RNA metabolism and the DDR.

2017-11-30 | PXD005913 | Pride

DNA damage responsive microRNAs misexpressed in human cancer regulate chemotherapy sensitivity (lung cancer cell lines)

Project description:The DNA damage response (DDR) is a cellular process that protects the genetic information against DNA damage and inhibits malignant transformation. Tumor cells are characterized by an aberrant DDR, which is exploited by genotoxic chemotherapy. However, cancer cells are able to develop drug resistance, for example by modulation of the DDR. Although the regulation of the DDR has been extensively studied, not much is known about the role of microRNAs (miRNAs). Here, we describe an approach to specifically identify DDR miRNAs in human primary epithelial cells that also play a role in tumorigenesis and response to cancer therapy in corresponding cancer cells. The miRNA expression profile was determined of 12 lung cancer cell lines.

2013-05-31 | E-GEOD-47524 | biostudies-arrayexpress

DNA damage responsive microRNAs misexpressed in human cancer regulate chemotherapy sensitivity (HMEpC & HSAEpC)

Project description:The DNA damage response (DDR) is a cellular process that protects the genetic information against DNA damage and inhibits malignant transformation. Tumor cells are characterized by an aberrant DDR, which is exploited by genotoxic chemotherapy. However, cancer cells are able to develop drug resistance, for example by modulation of the DDR. Although the regulation of the DDR has been extensively studied, not much is known about the role of microRNAs (miRNAs). We used an approach to specifically identify DDR miRNAs in human primary epithelial cells that also play a role in tumorigenesis and response to cancer therapy in corresponding cancer cells. The miRNA expression profile was determined in 132 samples: 2 primary epithelial cell types, 1 untreated sample, 4 genotoxic treated samples, 3 timepoints, 4 replicates each and 6 zero timepoints for each cell type

2013-05-31 | E-GEOD-47523 | biostudies-arrayexpress

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2013-05-31 | E-GEOD-47525 | biostudies-arrayexpress

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Project description:Numerous long noncoding RNAs (lncRNAs) are generated in response to external stimuli, but the scope and functions of such activity are not known. Here, we provide insight into how the transcription of lncRNAs are connected to DNA damage response by identifying a lncRNA ZFAS1, which is required for cell cycle arrest, transcription regulation and DNA repair. Mechanistically, ZFAS1 facilitates the changing hyperphosphorylated forms of the large subunit of RNAPII around transcription initiation sites by directly targeting the regulated genes. We revealed extensive transcription shutdown and concomitant stimulated engagement of RNAPII-Ser2P are crucial for repair and cell survival upon genotoxic stress. Finally, ZFAS1 knockout in mice dampened transcription-coupled nucleotide excision repair (TC-NER) and led to kidney dysplasia. Our study extends the understanding of lncRNAs in DNA damage repair (DDR) and implies a protective role of lncRNA against DDR-deficient developmental disorders.

2024-06-02 | GSE268446 | GEO

lncRNA-ZFAS1, an emerging gate-keeper in DNA damage-dependent transcriptional regulation [GRO-seq]

2024-06-02 | GSE268445 | GEO

lncRNA-ZFAS1, an emerging gate-keeper in DNA damage-dependent transcriptional regulation [CDK9 ChIP-Seq]

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lncRNA-ZFAS1, an emerging gate-keeper in DNA damage-dependent transcriptional regulation [OE CTD ChIP-Seq]

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Metabolic responses induced by DNA damage and poly (ADP-ribose) polymerase (PARP) inhibition in MCF-7 cells

Project description:Genomic instability is one of the hallmarks of cancer. Several chemotherapeutic drugs and radiotherapy induce DNA damage to prevent cancer cell replication. Cells in turn activate different DNA damage response (DDR) pathways to either repair the damage or induce cell death. These DDR pathways also elicit metabolic alterations which can play a significant role in the proper functioning of the cells. The understanding of these metabolic effects resulting from different types of DNA damage and repair mechanisms is currently lacking. In this study, we used NMR metabolomics to identify metabolic pathways which are altered in response to different DNA damaging agents. By comparing the metabolic responses in MCF-7 cells, we identified the activation of poly (ADP-ribose) polymerase (PARP) in methyl methanesulfonate (MMS)-induced DNA damage. PARP activation led to a significant depletion of NAD+. PARP inhibition using veliparib (ABT-888) was able to successfully restore the NAD+ levels in MMS-treated cells. In addition, double strand break induction by MMS and veliparib exhibited similar metabolic responses as zeocin, suggesting an application of metabolomics to classify the types of DNA damage responses. This prediction was validated by studying the metabolic responses elicited by radiation. Our findings indicate that cancer cell metabolic responses depend on the type of DNA damage responses and can also be used to classify the type of DNA damage.

2015-08-01 | MTBLS177 | MetaboLights

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