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Expression data of wild type, dDP mutant, and de2f1, deleted in the posterior, Drosophila 3rd instar larval eye imaginal discs

ABSTRACT: Apoptosis is an important process to eliminate cells from tissue which have incurred irreparable DNA damage. While dE2F1/dDP complexes respond to such damage by transcriptionally activating apoptotic genes, previous data suggests that activation of the previously characterized apoptotic target genes of dE2F1/dDP alone may not be the only gene regulation important for gamma irradiation-induced apoptosis. Here we report that following irradiation in dDP mutant 3rd instar larval eye imaginal discs, many genes important for oxidative phosphorylation are down-regulated, which are not down-regulated following irradiation in wild type eye discs.

ORGANISM(S): Drosophila melanogaster

PROVIDER: GSE39389 | GEO | 2013/11/25

SECONDARY ACCESSION(S): PRJNA170769

REPOSITORIES: GEO

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Expression data of wild type, dDP mutant, and de2f1, deleted in the posterior, Drosophila 3rd instar larval eye imaginal discs

Project description:Apoptosis is an important process to eliminate cells from tissue which have incurred irreparable DNA damage. While dE2F1/dDP complexes respond to such damage by transcriptionally activating apoptotic genes, previous data suggests that activation of the previously characterized apoptotic target genes of dE2F1/dDP alone may not be the only gene regulation important for gamma irradiation-induced apoptosis. Here we report that following irradiation in dDP mutant 3rd instar larval eye imaginal discs, many genes important for oxidative phosphorylation are down-regulated, which are not down-regulated following irradiation in wild type eye discs. Biological triplicates of wild type, dDP mutant and de2f1, deleted in the posterior, eye discs were untreated or irradiated with 40Gy of gamma radiation. Total RNA was extracted by Trizol from untreated eye discs and from irradiated eye discs 4h after irradiation. RNA was column purified. PCR amplified RNAs were hybridized on Affymetrix Drosophila Genome 2.0 Array.

2013-11-25 | E-GEOD-39389 | biostudies-arrayexpress

ChIP-seq using a Dp1 antibody in Drosophila S2R+ cells

Project description:Here we report the identification of genomic regions of DNA bound by Dp1 in Drosophila S2R+ cells. Dp1 is a dimerization partner of several E2F transcription factors and is needed for E2F target promoter binding. We find that Dp1 binds the promoter regions of genes important for oxidative phosphorylation. This result is important since our data demonstrates that expression of several oxidative phosphorylation genes is down-regulated in dDP mutant Drosophila 3rd instar larval eye imaginal discs. These ChIP-seq results suggest that the mechanism by which dDP regulates expression of these genes is direct. In addition, we have confirmed a number of these Dp1 bound gene promoters by conventional Chromatin Immunoprecipitation. Examination of Dp1 bound regions of genomic DNA in S2R+ cells.

2013-11-25 | E-GEOD-39393 | biostudies-arrayexpress

Gene expression analysis of Drosophila WT and dDP-/- mutant larvae.

Project description:WT and dDP-/- mutant larvae RNAs were analyzed on Drosophila 12 x 135 Nimbelgen gene expression microarrays. dDP-/- mutants are described in Frolov et al., 2001. Genes Dev. Aug 15;15(16):2146-60. PMID: 11511545 The complete elimination of E2F/DP function in Drosophila results in upregulation of DNA damage responses. The net effect of E2F regulation in larval tissues is that all classes of E2F target genes are reppressed by E2F/DP complexes.

2017-11-08 | GSE104544 | GEO

miRNA expression of lung cancer cells A549 and cisplatin (DDP) resistant lung cancer cells A549/DDP

Project description:To investigate the difference of miRNA expression between lung cancer cell A549 and its DDP-resistant cell strain A549/DDP, we have employed miRNA microarray expression to discover the difference expression of miRNAs of A549 cells and A549/DDP. We conducted RT-qPCR to examine the expression levels of top differential expressed miRNAs, namely, miR-197-5p, miR-4443, miR-642a-3p, miR-27b-3p and miR-100-5p, confirming low variability between two methods. The A549/DDP was established from A549 in our laboratory, by exposing A549 to gradually increasing DDP concentrations, until the final concentration at 1Î¼g/ml. To avoid the influence of drug to the A549/DDP cells, they were cultured in a drug-free medium for at least two weeks before gene expression analysis. miRNA expression of A549 and A549/DDP was then analzyed.

2016-08-16 | E-GEOD-85603 | biostudies-arrayexpress

LncRNA and mRNA expression profiling reveals the molecular mechanism of hyperthermia sensitizing human gastric cancer cisplatin- resistant cell line SGC-7901/DDP

Project description:Gastric cancer (GC) is the second leading cause of cancer-related death in the world, but due to the emergence of drug resistance, the chemotherapy effect of GC has not been improved. Hyperthermia (HT) can increase the sensitivity of tumor cells to chemotherapeutic drugs and cause the specific expression of related genes. Therefore, we want to confirm that HT can enhance the sensitivity of SGC-7901/DDP cells to cisplatin (DDP) and explore the molecular mechanism of sensitization. To study the optimal experimental conditions with synergistic effect, temperature gradients (41 ℃, 44 ℃, 47 ℃, 50 ℃), time gradients (12 h, 24 h, 36 h) and DDP concentration gradients (1 μg/ml, 2 μg/ml, 3 μg/ml) were established. Then the microarray analysis was performed to explore the molecular mechanism of HT sensitization. Our results showed that 47 ℃ HT+ 2 μg/ml DDP for 24 h could synergistically inhibit the proliferation of SGC7901/DDP cells and significantly promote early apoptosis. Differentially expressed lncRNAs and mRNAs between groups were obtained. ENST00000434470.1(IDI2-AS1), ENST00000592689.1(TTN-AS1) and ENST00000412526.1(LINC00161) may play a pro-apoptotic role, while asRNAs could be a potential target for the treatment of GC. KEGG pathway enrichment showed that DDP+HT may induce apoptosis of SGC7901/DDP cells through GPCR signaling pathway, BARD signaling pathway and TRAIL signaling pathway. In summary, HT can enhance the sensitivity of SGC-7901/DDP cells to DDP by activating related apoptotic genes and pathways.

2021-04-01 | GSE147385 | GEO

ChIP-seq using a Dp1 antibody in Drosophila S2R+ cells

2013-11-25 | GSE39393 | GEO

miRNA expression of lung cancer cells A549 and cisplatin (DDP) resistant lung cancer cells A549/DDP

2016-08-16 | GSE85603 | GEO

miRNA expression of exosomes derived from lung cancer cells A549 and cisplatin (DDP) resistant lung cancer cells A549/DDP

Project description:To investigate the difference of miRNA expression in exosomes derived from A549 cells and its DDP-resistant cell strain A549/DDP, we have employed miRNA microarray expression to discover the difference expression of miRNAs in exosomes derived from A549 and A549/DDP. We conducted RT-qPCR to examine the expression levels of top differential expressed miRNAs, namely, miR-197-5p, miR-4443, miR-642a-3p, miR-27b-3p and miR-100-5p, confirming low variability between two methods. The A549/DDP was established from A549 in our laboratory, by exposing A549 to gradually increasing DDP concentrations, until the final concentration at 1Î¼g/ml. To avoid the influence of drug to the A549/DDP cells, they were cultured in a drug-free medium for at least two weeks before gene expression analysis. After being incubated for 48-72h, the culture medium of cells was harvested. Exosomes were isolated by ultracentrifugation. And miRNA expression of exosomes derived from A549 and A549/DDP was then analzyed.

2016-08-16 | E-GEOD-85604 | biostudies-arrayexpress

miRNA expression of exosomes derived from lung cancer cells A549 and cisplatin (DDP) resistant lung cancer cells A549/DDP

2016-08-16 | GSE85604 | GEO

Chromosome copy number analysis (WGS) of repair-proficient and repair-deficient yeast strains (S. cerevisiae) after genotoxic treatment with camptothecin or X-ray irradiation

Project description:We investigated how yeast cells deficient in performing homologous recombination-mediated DNA repair due to a deletion of the critical RAD52 gene respond to irreparable DNA damage inflicted by genotoxic treatment commonly applied in cancer therapy (camptothecin and irradiation). We found that upon persistence of irreparable DNA damage, yeast rad52 mutants readily undergo checkpoint adaptation accompanied by the acquisition of resistance to further genotoxic insults as well as the development of aneuploidy. Together, our findings can be used to elucidate how repair-defective cancer cells can become treatment-resistant thereby providing a way to target these resistant cell clones by tackling their aneuploidy-associated phenotypes. To investigate these characteristics commonly present in aneuploid cells in our experimental set-up, we treated yeast cells with genotoxic agents and performed whole genome sequencing. We could identify frequent whole chromosome loss events manifesting in a sensitivity of cells to aneuploidy-targeting agents.

2019-10-22 | E-MTAB-7380 | biostudies-arrayexpress

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