Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA144095 | ENA |
REPOSITORIES: ENA
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Project description:microRNA regulates cellular responses to ionizing radiation (IR) through the translational control of target genes. We analyzed time-series changes in microRNA expressions upon γ-irradiation in H1299 lung cancer cell lines using microarray. Significantly changed microRNAs were selected based on ANOVA analysis, target genes of which were enriched to MAPK signaling pathway. Concurrent analysis of mRNA and microRNA uncovered that the expression of miR-26b and its target ATF2 mRNA were inversely correlated in γ-irradiated H1299 cells. The overexpression of miR-26b induced the suppression of ATF2 in γ-irradiated cells. When we inhibit the MAPK signaling pathway using SP600125, JNK inhibitor, the expression of miR-26b was induced even in γ-irradiated H1299 cells. From these results, we concluded that the expression of miR-26b was coordinated regulated by MAPK signaling pathway upon ionizing radiation, and MAPK signaling pathway was regulated by miR-26b in turn. We analyzed the time-series miRNA profiles of radioresistant H1299 cells in response to 2 Gy of ionizing radiation (IR) by performing quadratic regression (QR) analysis to identify genes associated with radioresistance
2011-09-13 | E-GEOD-30075 | biostudies-arrayexpress
Project description:microRNA regulates cellular responses to ionizing radiation (IR) through the translational control of target genes. We analyzed time-series changes in microRNA expressions upon γ-irradiation in H1299 lung cancer cell lines using microarray. Significantly changed microRNAs were selected based on ANOVA analysis, target genes of which were enriched to MAPK signaling pathway. Concurrent analysis of mRNA and microRNA uncovered that the expression of miR-26b and its target ATF2 mRNA were inversely correlated in γ-irradiated H1299 cells. The overexpression of miR-26b induced the suppression of ATF2 in γ-irradiated cells. When we inhibit the MAPK signaling pathway using SP600125, JNK inhibitor, the expression of miR-26b was induced even in γ-irradiated H1299 cells. From these results, we concluded that the expression of miR-26b was coordinated regulated by MAPK signaling pathway upon ionizing radiation, and MAPK signaling pathway was regulated by miR-26b in turn.
2011-09-14 | GSE30075 | GEO
Project description:Through the use of antagomiR-122, the knockdown of miR-122 was achieved with an efficiency of 70% in the cell line MCF-7RR with phenotype of acquired resistance to ionizing radiation. To evaluate the transcriptomic landscape resulting from knockdown of miR-122 of radioresistant breast cancer cells MCF-7RR. These assays showed the modulation of genes enrichment in RAS-MAPK and TNFR signaling pathways, inflammatory response and regulation of transcription.
2021-09-18 | GSE120171 | GEO
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.
2018-11-13 | GSE112375 | GEO
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.
2018-11-13 | GSE112374 | GEO
Project description:Mechanistic understanding of how ionizing radiation induces type I interferon signaling and how to amplify this signaling module should help to maximize the efficacy of radiotherapy. In the current study, we report that inhibitors of the DNA damage response kinase ATR can significantly potentiate ionizing radiation-induced innate immune responses. Using a series of mammalian knockout cell lines, we demonstrate that, surprisingly, both the cGAS/STING-dependent DNA-sensing pathway and the MAVS-dependent RNA-sensing pathway are responsible for type I interferon signaling induced by ionizing radiation in the presence or absence of ATR inhibitors. The relative contributions of these two pathways in type I interferon signaling depend on cell type and/or genetic background. We propose that DNA damage-elicited double-strand DNA breaks releases DNA fragments, which may either activate the cGAS/STING-dependent pathway or-especially in the case of AT-rich DNA sequences-be transcribed and initiate MAVS-dependent RNA sensing and signaling. Together, our results suggest the involvement of two distinct pathways in type I interferon signaling upon DNA damage. Moreover, radiation plus ATR inhibition may be a promising new combination therapy against cancer.
2020-05-07 | GSE150003 | GEO
Project description:To further investigate the potential molecular basis of the protective effects of HSC on irradiation (6.5Gy) damage, gene expression analysis was conducted on rats liver tissues using microarrays.Pre-treatment with HSC prevented differential expression of 66% (1,398 genes) of 2,126 genes differentially expressed in response to radiation. Pathway enrichment analysis indicated that these genes were mainly involved in a total of 32 pathways, such as olfactory transduction, uroactive ligand-receptor interaction, pathways in cancer, calcium signaling pathway, vascular smooth muscle contraction, cytokine-cytokine receptor interaction, mitogen-activated protein kinase (MAPK) signaling pathway, peroxisomal proliferator-activated receptor (PPAR）signaling pathway, gonadotropin-releasing hormone (GnRH) signaling pathway, Wnt signaling pathway, janus kinase-signal transducers and activators of transcription (Jak-STAT) signaling pathway, Notch signaling pathway.Our analysis indicated that the pretreatment of rats with HSC attenuated radiation-induced these pathways, such as multiple MAPK pathways, suggesting that the protective effect of HSC acts mainly through the attenuation of these pathways. The rats were randomly assigned to one of the three following treatment groups (10-12 animals per group): normal control, radiation and HSC dose (10g/kg body weight/day) + radiation. HSC dissolved in double distilled water were administered intragastrically to the male animals for 3 consecutive days before irradiation. Radiation induced gene expression in rat liver was measured at 24 hours after 6.5 Gy exposure.
2014-05-15 | E-GEOD-57692 | biostudies-arrayexpress
Project description:Genetic background modulates lincRNA-coordinated tissue response to low dose ionizing radiation
| PRJNA264740 | ENA
Project description:Accidental or deliberate ionizing radiation exposure is fatal due to widespread hematopoietic destruction. However, little is known about either the course of injury or the definitive molecular pathways that regulate the subsequent regenerative response. We have investigated the spatial and temporal consequences of radiation injury on the hematopoietic system and show the Wnt signaling pathway is critially important for regeneration.
2016-08-31 | GSE50620 | GEO
Project description:The involvement the thioredoxin system in radiation resistance was investigated in human lung cancer cells by a combination of ionizing radiation and specific thioredoxin reductase-inhibition by a phosphine gold compound. Gene expression profiles (Human Gene 1.0 ST) of lung cancer cells subjected to ionizing radiation and/or inhibition of thioredoxin reductase were studied. Data analyses were performed using the Affymetrix GeneChip Operating Software (GCOS) Version 1.4.
2010-12-03 | E-GEOD-25814 | biostudies-arrayexpress