MiRNA expression profiling of gamma-irradiated A549 cells at 4 h after irradiation
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE112374 | GEO | 2018/11/13
REPOSITORIES: GEO
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Project description:We analyzed the combination of ionizing radiation (IR, 2.0 Gy) along with microRNA-mediated targeting of genes involved in DSB repair to sensitize human non-small cell lung cancer (NSCLC) cells.
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Project description:DNA-Double strand breaks (DSBs) generated by radiation therapy represent the most efficient lesions to kill tumor cells, however, the inherent DSB repair efficiency of tumor cells can cause cellular radioresistance and impact on therapeutic outcome. Genes of DSB repair represent a target for cancer therapy since their down-regulation can impair the repair process making the cells more sensitive to radiation. In this study, we analyzed the combination of ionizing radiation (IR) along with microRNA-mediated targeting of genes involved in DSB repair to sensitize human non-small cell lung cancer (NSCLC) cells. MicroRNAs are natural occurring modulators of gene expression and therefore represent an attractive strategy to affect the expression of DSB repair genes. As possible IR-sensitizing targets genes we selected genes of homologous recombination (HR) and non-homologous end joining (NHEJ) pathway (i.e. RAD51, BRCA2, PRKDC, XRCC5, LIG1). We examined these genes to determine whether they may be real targets of selected miRNAs by functional and biological validation. The in vivo effectiveness of miRNA treatments has been examined in cells over-expressing miRNAs and treated with IR. Taken together, our results show that hsa-miR-96-5p and hsa-miR-874-3p can directly regulate the expression of target genes. When these miRNAs are combined with IR can decrease the survival of NSCLC cells to a higher extent than that exerted by radiation alone, and similarly to radiation combined with specific chemical inhibitors of HR and NHEJ repair pathway. This SuperSeries is composed of the SubSeries listed below.
2018-11-13 | GSE112376 | GEO
Project description:We aim at understanding how ionizing radiations (IR) increase the risk of developing myeloid leukemia. We recently showed that IR leads to the derepression of retroelements. We demonstrated that retroelements expression in aged HSCs is regulated by the heterochromatin repressive histone mark H3K9me3. However, the mechanisms by which IR specifically triggers retroelements expression in HSCs are unknown. We hypothesized that retroelements derepression is due to IR-induced heterochromatin changes. To answer this question, we performed H3K9me3 ChIP-seq experiments in hematopoietic stem cells sorted from mice one month after they were irradiated and compared them to controls hematopoietic stem cells sorted from non-irradiated mice.
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Project description:We used microarrays to measure the expression levels of genes in irradiated immortalized B cells, lymphoblastoid cells, from members of Centre dEtude du Polymorphisme Humain (CEPH) Utah pedigrees. Data were collected for cells at baseline and 2 hour and 6 hour after exposure to 10 Gy of ionizing radiation (IR). Experiment Overall Design: We used microarrays to measure the expression levels of genes in irradiated immortalized B cells, lymphoblastoid cells, from members of 15 Centre dEtude du Polymorphisme Humain (CEPH) Utah pedigrees (CEPH 1333, 1341, 1346, 1362, 1408, 1416, 1420, 1421, 1423, 1424, 1444, 1447, 1451, 1454, 1582). Expression data was obtained for cell lines derived from 2 parents and 8 children per each family. Cells were irradiated at 10 Gy in a 137Cs irradiator. Cells were harvested prior to radiation and at 2 and 6 hours following exposure to IR.
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Project description:We aim at understanding how ionizing radiations (IR) increase the risk of developing myeloid leukemia. We recently showed that IR leads to the derepression of retroelements. Retroelements are major contributors of gene regulatory networks. However, the impact of retroelements derepression on the HSC transcriptome and function remains to be addressed. We hypothesized that retroelements derepression is involved in HSC transcriptomic alterations. To answer this question, we performed RNA-seq experiments in hematopoietic stem cells sorted from mice one month after they were irradiated and compared them to controls hematopoietic stem cells sorted from non-irradiated mice.
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Project description:Recent observations show that the single-cell response of p53 to ionizing radiation (IR) is “digital” in that it is the number of oscillations rather than the amplitude of p53 that shows dependence on the radiation dose. We present a model of this phenomenon. In our model, double-strand break (DSB) sites induced by IR interact with a limiting pool of DNA repair proteins, forming DSB–protein complexes at DNA damage foci. The persisting complexes are sensed by ataxia telangiectasia mutated (ATM), a protein kinase that activates p53 once it is phosphorylated by DNA damage. The ATM-sensing module switches on or off the downstream p53 oscillator, consisting of a feedback loop formed by p53 and its negative regulator, Mdm2. In agreement with experiments, our simulations show that by assuming stochasticity in the initial number of DSBs and the DNA repair process, p53 and Mdm2 exhibit a coordinated oscillatory dynamics upon IR stimulation in single cells, with a stochastic number of oscillations whose mean increases with IR dose. The damped oscillations previously observed in cell populations can be explained as the aggregate behavior of single cell
2020-05-13 | MODEL2005130001 | BioModels
Project description:This analysis compares the signal of DNA from T-cell lymphoblastic lymphomas induced by gamma-irradiation versus normal thymuses Keywords: Tumor profiles, comparison of tumoral versus wilf-type tissues, lymphomas and leukemias C57BL/6J animals were maintained in our animal facilities following the appropriate ethical recommendations from our institutions. For tumor induction, 4-week-old mice of both sexes were exposed to four weekly doses of 1.75 Gy/dose of ionizing gamma radiation. Treated mice were observed daily until moribund, then sacrificed and autopsied. DNA, RNA and proteins were isolated from these samples using routine procedures.
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Project description:The goal of this project was to analyze gene expression changes upon DNA damage induced by ionizing radiation (IR). To this end, human U-2 OS cells were left untreated or exposed to 4 Gy of IR and 24 h after IR exposure collected for RNA extraction and sequencing.
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Project description:Accidents with ionizing radiation (IR) often involve acute high dose exposures that can lead to acute radiation syndrome and late effects. IR can induce genomic lesions, cell death or carcinogenesis. Here, we investigated acute IR-induced cellular genomic signatures at the genome wide level. After exposing the adenocarcinoma cell line A549 to an acute 6 Gy 240 kV X-Ray dose, four surviving clonogenic cells were recovered by minimal dilution and further expanded and analyzed by cytogenetics, chromosome painting and tiling-path array CGH, with the non-irradiated clone0 serving as control. It was found that acute X-ray exposure induced changes in modal chromosome number and specific translocations in the four irradiation surviving clones. Furthermore, clone4 displayed an increased radiosensitivity at D > 5 Gy. Array CGH disclosed unique and recurrent genomic changes, predominantly gains, and disclosed fragile sites FRA3B and FRA16D as preferential regions of genomic alterations in all irradiated clones, which likely relates to irradiation-induced genomic stress. Gene expression analysis revealed a specific profile of 364 genes in clone4, of which p53 pathway genes may contribute to its increased radiosensitivity. IR-induced genomic changes AND fragile site expression highlight the capacity of a single acute radiation exposure to resculpture the genome of tumor cells by inflicting genomic stress.
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