MicroRNA Expression data from human Ewing's sarcoma (ES)
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Masanori Kawano
PROVIDER: E-GEOD-70825 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:To explore possible oncogenic factors in ES, we used a microarray-based approach to profile changes in the expression of mRNAs in five ES cell lines and human mesenchymal stem cells (hMSCs). We used a microarray-based approach to profilein the mRNA expression of ES Human ES cell lines were analyzed with genome-wide expression arrays.
2015-07-14 | E-GEOD-70826 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series
2015-07-14 | E-GEOD-70827 | biostudies-arrayexpress
Project description:To explore possible oncogenic factors in OS, we used a microarray-based approach to profile changes in the expression of mRNAs in five OS cell lines and human mesenchymal stem cells (hMSCs). We used a microarray-based approach to profile the mRNA expression of OS Human OS cell lines were analyzed with genome-wide expression arrays.
2015-07-01 | E-GEOD-70414 | biostudies-arrayexpress
Project description:To explore possible oncogenic factors in OS, we used a microarray-based approach to profile changes in the expression of miRNAs in five OS cell lines and human mesenchymal stem cells (hMSCs). We used a microarray-based approach to profile in the miRNA expression of OS Human OS cell lines were analyzed with genome-wide expression arrays.
2015-07-01 | E-GEOD-70367 | biostudies-arrayexpress
Project description:Microarray gene expression analysis conducted from cell lines in each of three cohorts: (1) Resistant ES cell lines, (2) Sensitive parental ES cell lines treated with YK-4-279 for 72 hours, and (3) untreated sensitive parental ES cell lines (Three replicates from TC32 & TC71 original parental cell lines) We used microarrays to detail the global programme of gene expression underlying mechanism of resistance to YK-4-279 within parental sensitive and resistant selected Ewing's Sarcoma cell lines. We identified distinct classes of up-regulated genes during this process. Total RNA was extracted from the cell lines using the Qiagen miRNeasy Mini kit. RNA quality was assessed to have an RNA integrity number before amplification and labeling using AffymetrixM-bM-^@M-^Ys GeneChip GeneChipM-BM-.3M-bM-^@M-^Y IVT Express Kit following manufacturerM-bM-^@M-^Ys instructions. Amplified and biotinylated cRNAs were hybridized onto Affymetrix GeneChip Human Genome U133A 2.0 cartridge arrays, Washed, and Stained with kit following manufacturerM-bM-^@M-^Ys instructions. Arrays were scanned using Affymetrix GeneChip Scanner 3000 and the initial raw data were extracted using Affymetrix GeneChip Command Console-Expression software. The statistical analyses of scanned data were performed using default setting on GeneSpring GX 12.1 software (Agilent).
2014-09-04 | E-GEOD-61042 | biostudies-arrayexpress
Project description:To explore possible oncogenic factors in ES, we used a microarray-based approach to profile changes in the expression of mRNAs in five ES cell lines and human mesenchymal stem cells (hMSCs). We used a microarray-based approach to profilein the mRNA expression of ES
2015-07-14 | GSE70826 | GEO
Project description:To explore possible oncogenic factors in ES, we used a microarray-based approach to profile changes in the expression of miRNAs in five ES cell lines and human mesenchymal stem cells (hMSCs). We used a microarray-based approach to profilein the mRNA expression of ES
2015-07-14 | GSE70825 | GEO
Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series
2015-07-01 | E-GEOD-70415 | biostudies-arrayexpress
Project description:The synthesis and processing of mRNA, from transcription to translation initiation, often requires splicing of intragenic material. The final mRNA composition varies based upon proteins that modulate splice site selection. EWS-FLI1 is an Ewing sarcoma (ES) oncogene with an interactome that we demonstrate to have multiple partners in spliceosomal complexes. We evaluate EWS-FLI1 upon post-transcriptional gene regulation using both exon array and RNA-seq. Genes that potentially regulate oncogenesis including CLK1, CASP3, PPFIBP1, and TERT validate as alternatively spliced by EWS-FLI1. EWS-FLI1 also alters splicing by directly binding to known splicing factors including DDX5, hnRNPK, and PRPF6. Reduction of EWS-FLI1 produces an isoform of g-TERT that has increased telomerase activity compared to WT TERT. The small molecule YK-4-279 is an inhibitor of EWS-FLI1 oncogenic function that disrupts specific protein interactions including DDX5 and RNA helicase A (RHA) that alters RNA splicing ratios. As such, YK-4-279 validates the splicing mechanism of EWS-FLI1 showing alternatively spliced gene patterns that significantly overlap with EWS-FLI1 reduction and WT human mesenchymal stem cells. Exon array analysis of 75 ES patient samples show similar isoform expression patterns to cell line models expressing EWS-FLI1, supporting the clinical relevance of our findings. These experiments establish systemic alternative splicing as an oncogenic process modulated by EWS-FLI1. EWS-FLI1 modulation of mRNA splicing may provide insight into the contribution of splicing towards oncogenesis, and reciprocally, EWS-FLI1 interactions with splicing proteins may inform the splicing code. Alternative splicing of RNA allows a limited number of coding regions in the human genome to produce proteins with diverse functionality. Alternative splicing has also been implicated as an oncogenic process. Identifying aspects of cancer cells that differentiate them from non-cancer cells remains an ongoing challenge and our research suggests that alternatively spliced mRNA and subsequent protein isoforms will provide new anti-cancer targets. We determined that the key oncogene of Ewing sarcoma (ES), EWS-FLI1, regulates alternative splicing in multiple cell line models. These experiments establish oncogenic aspects of splicing which are specific to cancer cells and thereby illuminate potentially oncogenic splicing shifts as well as provide a useful stratification mechanism for ES patients. We analyzed three models of EWS-FLI1 using Affymetrix GeneChip Human Exon 1.0 ST microarray: (i) Ewing's sarcoma TC32 wild-type cells expressing EWS-FLI1, and TC32 cells where EWS-FLI1 was reduced with a lentiviral shRNA; (ii) A673i, which has a doxycycline-inducible shRNA to reduce EWS-FLI1 expression, and wild-type EWS-FLI1 to screen for alternative splicing as measured by exon-specific expression changes; and (iii) human mesenchymal stem cells (hMSC), a putative cell of origin of Ewing's sarcoma, exogenously expressing EWS-FLI1, and hMSC wild-type cells without EWS-FLI1. Three biological replicates were included for each condition. The Bioconductor package "oligo" in the R programming language was used for normalization and background correction. Analysis was carried out using only core probesets, as defined by the manufacturer.
2015-03-31 | E-GEOD-65941 | biostudies-arrayexpress
Project description:Ewing’s sarcoma (ES) is a highly aggressive bone tumor, and the second most prevalent pediatric bone malignancy. The presence of metastasis at diagnosis decreases the three-year survival rate to 20% and contributes to diminished prognosis. Researches are indispensable for the early characterization of the disease and prediction of metastatic-prone patients, through biomarkers identification. Moreover, there is currently no available data on ES utilizing non-biopsy samples, such as plasma. This study utilizes a proteomic analysis of Ewing's sarcoma patient’s plasma samples and biopsies. Initially, the ES group was compared with the control counterpart. In a next step, the ES arm was further stratified into either initially metastatic and non-metastatic, or poor and good chemotherapy responder groups to identify protein expression profiles that can predict metastatic proneness and chemotherapy response, respectively.
2023-12-19 | PXD035812 | Pride