RNA-seq analysis using A549 cells with FXR knockdown and control A549 cells with or without ionizing radiation treatment.
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ABSTRACT: 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:In this study, we explored the role of TRIM22 in the response to ionizing radiation (IR) in A549 human lung cancer cells. TRIM22 was stably knocked down in A549 cells using shRNA, and four experimental groups were established: control A549 cells (non-irradiated), control A549 cells (irradiated), TRIM22 knockdown A549 cells (non-irradiated), and TRIM22 knockdown A549 cells (irradiated). RNA sequencing (RNA-seq) was performed to identify gene expression changes associated with TRIM22 knockdown and irradiation. This dataset provides insights into the molecular mechanisms by which TRIM22 influences the cellular response to radiation and its potential impact on cancer therapy.
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:Densely ionizing radiation is a major component of the space radiation environment and has potentially greater carcinogenic effect compared to sparsely ionizing radiation that is prevalent in the terrestrial environment. It is unknown to what extent the irradiated microenvironment contributes to the differential carcinogenic potential of densely ionizing radiation. To address this gap, 10-week old BALB/c mice were irradiated with 100 cGy sparsely ionizing g-radiation or 10, 30, or 80 cGy of densely ionizing, 350 MeV/amu Si particles and transplanted 3 days later with syngeneic Trp53 null mammary fragments. Tumor appearance was monitored for 600 days. Tumors arising in Si-particle irradiated mice had a shorter median time to appearance, grew faster and were more likely to metastasize. Most tumors arising in sham-irradiated mice were ER-positive, pseudo-glandular and contained both basal keratin 14 and luminal keratin 8/18 cells (designated K14/18), while most tumors arising in irradiated hosts were K8/18 positive (designated K18) and ER negative. Comparison of K18 vs K14/18 tumor expression profiles showed that genes increased in K18 tumors were associated with ERBB2 and KRAS while decreased genes overlapped with those down regulated in metastasis and by loss of E-cadherin. Consistent with this, K18 tumors grew faster than K14/18 tumors and more mice with K18 tumors developed lung metastases compared to mice with K14/18 tumors. However, K18 tumors arising in Si-particle irradiated mice grew even faster and were more metastatic compared to control mice. A K18 Si-irradiated host profile was enriched in genes involved in mammary stem cells, stroma, and Notch signaling. Thus systemic responses to densely ionizing radiation enriches for a ER-negative, K18-positive tumor, whose biology is more aggressive compared to similar tumors arising in non-irradiated hosts. Key Words: ionizing radiation; breast cancer; heavy ion radiation;initiation; promotion
Project description:Densely ionizing radiation is a major component of the space radiation environment and has potentially greater carcinogenic effect compared to sparsely ionizing radiation that is prevalent in the terrestrial environment. It is unknown to what extent the irradiated microenvironment contributes to the differential carcinogenic potential of densely ionizing radiation. To address this gap, 10-week old BALB/c mice were irradiated with 100 cGy sparsely ionizing g-radiation or 10, 30, or 80 cGy of densely ionizing, 350 MeV/amu Si particles and transplanted 3 days later with syngeneic Trp53 null mammary fragments. Tumor appearance was monitored for 600 days. Tumors arising in Si-particle irradiated mice had a shorter median time to appearance, grew faster and were more likely to metastasize. Most tumors arising in sham-irradiated mice were ER-positive, pseudo-glandular and contained both basal keratin 14 and luminal keratin 8/18 cells (designated K14/18), while most tumors arising in irradiated hosts were K8/18 positive (designated K18) and ER negative. Comparison of K18 vs K14/18 tumor expression profiles showed that genes increased in K18 tumors were associated with ERBB2 and KRAS while decreased genes overlapped with those down regulated in metastasis and by loss of E-cadherin. Consistent with this, K18 tumors grew faster than K14/18 tumors and more mice with K18 tumors developed lung metastases compared to mice with K14/18 tumors. However, K18 tumors arising in Si-particle irradiated mice grew even faster and were more metastatic compared to control mice. A K18 Si-irradiated host profile was enriched in genes involved in mammary stem cells, stroma, and Notch signaling. Thus systemic responses to densely ionizing radiation enriches for a ER-negative, K18-positive tumor, whose biology is more aggressive compared to similar tumors arising in non-irradiated hosts. Key Words: ionizing radiation; breast cancer; heavy ion radiation;initiation; promotion 3 different dose of Si were used. Total RNA was extracted from mammary tumors derived from transplantations of non-irradiated p53null mammary fragments into irradiated hosts. We analyzed a total of 45 Trp53-null tumors: 18 from sham-irradiated hosts, 9 from 10 cGy Si-irradiated hosts, 10 from 30 cGy Si-irradiated hosts, and 8 from irradiated hosts.
Project description:Back skin from 8-10 weeks male mice was plucked to induce actively growing hair follicles. After 9 days, the back skin was irradiated with 5Gy ionizing radiation. Skin samples were collected for CHIP-seq analysis using a p53 antibody and H3K4me3 antibody. We compared wild type and Krt17 knock out mice for their epigenetic regulation of gene expression change in response to ionizing radiation
Project description:The goal of the study is to identify differentially expressed isoforms in response to SRSF1 knockdown and/or ionizing radiation in HEK293T cells
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