Transcriptome analysis of dissected tumour tissue from Drosophila melanogaster larval tumour models in CD compared to HSD.
Ontology highlight
ABSTRACT:
ORGANISM(S): Drosophila melanogaster
PROVIDER: GSE139957 | GEO | 2020/07/28
REPOSITORIES: GEO
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Project description:Transcriptome analysis of dissected tumour tissue from Drosophila melanogaster larval tumour models in CD compared to HSD.
| PRJNA587732 | ENA
Project description:The study was conducted to identify differentially expressed genes in 1) whole flies that were fed a high sugar diet (HSD), in comparison to flies treated with control diet (CD), and 2) HSD male line derived F1 and F2 progenies, compared to that derived through CD male line. The ancestral HSD exposure of F1 or F2 flies was thus limited only to F0 males. However, besides comparing F1 and F2 flies raised on CD, the F1 and F2 flies treated with HSD were also compared. F0 HSD females were profiled but not used for the mating purpose.
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Project description:Transcriptomic profiling along a time course of muscle wasting revealed a progressive deregulation of muscle structure and organisation. An array of molecular signatures were associated with this deregulation, including a perturbed ubiquitin-proteasome system, an increase in the unfolded protein response, and an increase in MAPK pathway signalling.
2020-07-28 | GSE139955 | GEO
Project description:To investigate the mRNA expression of purified tumour-infiltrating M-MDSCs from the NSD or HSD group, we employed Agilent Whole Genome Oligo Microarrays (one-color) as a discovery platform to identify differentially expressed genes (DEGs) between NSD and HSD group. We identified 5391 differentially expressed genes (DEGs) comprising 2586 upregulated and 2805 downregulated genes with a fold change greater than 1.5 between M-MDSCs from the NSD and HSD groups. Subsequently, the results demonstrated a significant shift towards an antitumour pro-inflammatory phenotype in HSD-fed mice with a dominant increase in NOS2, TNF, IL-12a, Toll-like receptor 4 (TLR4) and chemokine (C-C motif) ligand 19 (CCL19) expression and a decrease in lymphocyte antigen 6 complex, locus C1 (Ly6C1), C-C-C motif chemokine ligand 12 (CXCL12), indoleamine 2,3-dioxygenase 1 (IDO1) and CCL2 expression. Among these differences, the difference in the expression of IL-12, TNF-α, NOS2, IL-10 and arginase 1 (Arg1) was confirmed by ELISA or qRT-PCR . Meanwhile, the 2,586 DEGs upregulated (fold change >1.5) in M-MDSCs from the HSD group were markedly enriched in processes involving cytokine production, cell chemotaxis, INF-γ production, cell maturation, osmotic stress responses, acute inflammatory responses, etc. In addition, Analysis of the microarray dataset indicated that the expression of 2 key TFs (activating transcription factor 2 [ATF2] and NFAT5) responsible for osmotic stress was enhanced in the M-MDSCs from the HSD group . We further found that NFAT5 expression was significantly upregulated in M-MDSCs from the HSD group but that there was no difference in ATF2 expression between the two groups in both tumour models.
2020-02-14 | GSE125430 | GEO
Project description:We profile the binding of Steroid Receptor Co-activator (SRC1) in LY2 cells, a tamoxifen-resistant cell line, in the presence and absence of tamoxifen using ChIP-sequencing technology. The development of breast cancer resistance to endocrine therapy results from an increase in cellular plasticity leading to the development of a steroid-independent tumour. The p160 steroid coactivataor protein SRC-1, through interactions with developmental proteins and other non-steroidal transcription factors, drives this tumour adaptability. Here, using discovery studies, we identify ADAM22, a non-protease member of the ADAMs family, as a direct, ER-independent target of SRC-1. Molecular, cellular and in vivo studies confirmed SRC-1 as a regulator of ADAM22. At a functional level, a role for ADAM22 in cellular migration and differentiation was observed. In vivo data from a mouse xenograft model indicated that ADAM22 expression was higher in 4-OHT-treated endocrine-resistant tumours than in tumours derived from isogenic, sensitive cells. Furthermore, in breast cancer patients, ADAM22 expression is an independent predictor of poor disease free survival. SRC-1 can function as a molecular switch which converts a steroid-responsive tumour to a steroid-resistant tumour. The ER-independent SRC-1 target ADAM22 is a potential drug target and a companion predictive biomarker in the treatment of endocrine-resistant breast cancer. Examination of SRC-1 binding in LY2 cells in the presence or absence of tamoxifen treatment. 2 replicates each.
2011-11-01 | E-GEOD-28987 | biostudies-arrayexpress
Project description:8 week-old male Hsd:ICR(CD-1) mice were fed ad libitum a standard chow (Harlan Teklad diet 2018S) and housed in groups of five. Animals were then divided into 3 pools (n=10) and sacrificed. The small intestine was extracted and divided into three sections, where the first 2-3 cm after the stomach comprised the duodenum, the middle third the jejunum, and the section before the ileo-ceco-colic junction comprised the ileum. Colon was not divided into proximal and distal sections and was treated as a single intestinal section.
2007-12-13 | E-GEOD-849 | biostudies-arrayexpress
Project description:We profile the binding of Steroid Receptor Co-activator (SRC1) in LY2 cells, a tamoxifen-resistant cell line, in the presence and absence of tamoxifen using ChIP-sequencing technology. The development of breast cancer resistance to endocrine therapy results from an increase in cellular plasticity leading to the development of a steroid-independent tumour. The p160 steroid coactivataor protein SRC-1, through interactions with developmental proteins and other non-steroidal transcription factors, drives this tumour adaptability. Here, using discovery studies, we identify ADAM22, a non-protease member of the ADAMs family, as a direct, ER-independent target of SRC-1. Molecular, cellular and in vivo studies confirmed SRC-1 as a regulator of ADAM22. At a functional level, a role for ADAM22 in cellular migration and differentiation was observed. In vivo data from a mouse xenograft model indicated that ADAM22 expression was higher in 4-OHT-treated endocrine-resistant tumours than in tumours derived from isogenic, sensitive cells. Furthermore, in breast cancer patients, ADAM22 expression is an independent predictor of poor disease free survival. SRC-1 can function as a molecular switch which converts a steroid-responsive tumour to a steroid-resistant tumour. The ER-independent SRC-1 target ADAM22 is a potential drug target and a companion predictive biomarker in the treatment of endocrine-resistant breast cancer.
2011-11-01 | GSE28987 | GEO
Project description:Colon gene expression in human IBD. The three major clinical subsets of Inflammatory Bowel Disease (IBD) include colon-only Crohn's Disease (CD), ileo-colonic CD, and Ulcerative Colitis (UC). These experiments tested differential colon gene expression in these three types of IBD, relative to healthy control samples, and the local degree of mucosal inflammation as measured by the CD Histological Index of Severity (CDHIS). Colon biopsy samples were obtained from IBD patients at diagnosis and during therapy, and healthy controls. The global pattern of gene expression was determined using GeneSpring software, with a focus upon candidate genes identified in a recent genome wide association study in pediatric onset IBD. Data suggested that two of these candidate genes are up regulated in pediatric IBD, partially influenced by local mucosal inflammation. These experiments tested differential colon gene expression in healthy, CD, and UC samples for candidate genes identified in a recent pediatric onset IBD genome wide association study. Keywords: Single time point in CD and UC and healthy controls.
2009-03-11 | GSE10616 | GEO
Project description:Single nucleotide polymorphisms (SNPs) and copy number variants (CNVs) are found at different rates in human cancer. To determine if these genetic lesions appear in Drosophila tumors we have sequenced the genomes of 17 malignant neoplasms caused by mutations in l(3)mbt, brat, aurA, or lgl We have found CNVs and SNPs in all the tumors. Tumor-linked CNVs range between 11 and 80 per sample, affecting between 92 and 1546 coding sequences. CNVs are in average less frequent in l(3)mbt than in brat lines. Nearly half of the CNVs fall within the 10 to 100Kb range, all tumor samples contain CNVs larger that 100 Kb and some have CNVs larger than 1Mb. The rates of tumor-linked SNPs change more than 20-fold depending on the tumor type: at late time points brat, l(3)mbt, and aurA and lgl lines present median values of SNPs/Mb of exome of 0.16, 0.48, and 3.6, respectively. Higher SNP rates are mostly accounted for by C > A transversions, which likely reflect enhanced oxidative stress conditions in the affected tumors. Both CNVs and SNPs turn over rapidly. We found no evidence for selection of a gene signature affected by CNVs or SNPs in the cohort. Altogether, our results show that the rates of CNVs and SNPs, as well as the distribution of CNV sizes in this cohort of Drosophila tumors are well within the range of those reported for human cancer. Genome instability is therefore inherent to Drosophila malignant neoplastic growth at a variable extent that is tumor type dependent.
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Project description:Cachexia is a systemic wasting syndrome that develops in many cancers and increases mortality. Despite its importance, it is largely unknown how cachexia progressively and differentially induces tissue wasting. Although cachexia occurs also in pediatric patients, little is known on the underlying mechanisms. Here, we have used pediatric melanoma xenografts to determine the progression and tissue-specific impact of juvenile cachexia on skeletal muscles, heart, white and brown adipose, liver, and brain. We find that the heart and muscles undergo wasting at early stages and are the tissues most strongly impacted transcriptionally. Beyond wasting, we identify general and organ-specific transcriptional changes that likely indicate derangement of organ/tissue function by cachexia. Moreover, also the transcriptome of tissues that do not undergo wasting, such as the brain, is profoundly remodeled by cachexia. Altogether, this study provides insight into the progression of melanoma-induced pediatric cachexia and its differential impact on distinct organ systems.
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