Project description:To seek if ionizing radiation have different biological effect on lung normal cells and cancer cells, we treated lung epithelial cell line BEAS-2B, non-small cell lung cancer cell line A549 and small cell lung cancer cell line H446 with 10 Gy X-ray radiation
Project description:In this study, we explored the role of FXR in the response to ionizing radiation (IR) in A549 human lung cancer cells. FXR was stably knocked down in A549 cells using shRNA, and four experimental groups were established: control A549 cells (non-irradiated), control A549 cells (irradiated), FXR knockdown A549 cells (non-irradiated), and FXR knockdown A549 cells (irradiated). RNA sequencing (RNA-seq) was performed to identify gene expression changes associated with FXR knockdown and irradiation. This dataset provides insights into the molecular mechanisms by which FXR influences the cellular response to radiation and its potential impact on cancer therapy.
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
Project description:We have employed microarray expression profiling as a discovery platform to identify microRNAs induced by radiation. Human A549 lung cancer cells were irradiated (2Gy/day for consistent 3days) and miRNA signature was identified that distinguished between control and radiation treated samples.Irradiated and un-irradiated A549 cells were harvested after 48 hr of treatment and microarray analysis was performed. Expression of five miRNAs (miR-30a, miR-30b, miR-30c, miR-30d, and miR-30d) from this signature was quantified in the same RNA samples by real-time PCR, confirming variability between control and radiation treated A549 cells.
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.
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.
Project description:To identify radiation-induced miRNAs, we initially profiled human miRNA expression in NSCLC A549 and H1299 cells treated with X-ray radiation using miRNA microarrays. Indeed, we observed multiple dysregulated miRNAs following radiation in NSCLC cell lines.
