Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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MicroRNA expression data from Ewing's sarcoma tumor samples

ABSTRACT: Ewing sarcoma a rare pediatric tumor characterized by EWSR1-ETS fusions. We performed expression profiling of both miRNA and mRNA from the same Ewing's sarcoma tumors. We propose a novel statistical measure of non-linear dependence between miRNA and mRNA expression, In order to infer miRNA-target interactions. This approach, That we name antagonism pattern detection, Is based on the statistical recognition of a triangular-shaped pattern in miRNA-target expression profiles. This pattern is observed in miRNA-target expression measurements since their simultaneously elevated expression is statistically under-represented in the case of miRNA silencing effect. The proposed method enables miRNA target prediction to strongly rely on cellular context and physiological conditions reflected by expression data. Total RNAs issued of 39 Ewing tumors were used for mRNA and miRNA microarray analyses. The microRNA data were collected using the Illumina human-6 V1 BeadChip.

ORGANISM(S): Homo sapiens

SUBMITTER: Loredana Martignetti

PROVIDER: E-GEOD-37370 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:Disease relapse and resistance to chemotherapy represent challenging issues in a subset of Hodgkin Lymphoma (HL) patients. Activity and mechanism(s) of action of a novel PI3K/ERK dual inhibitor AEZS-136 (Ãterna Zentaris GmbH, Germany, EU) were examined in L-540, SUP-HD1, KM-H2 and L-428 cell lines. Despite exposure to AEZS-136 induced a significant cell growth inhibition (range, 30-80%), levels of caspase-independent cell death and mitochondrial dysfunction, were only observed in L-540 (62 Â±9 vs 14 Â±3%, P â¤.0001) and SUP-HD1 (46 Â±2% vs 15 Â±2%, P â¤.0001) cells. Gene expression profiling indicated that the effects of AEZS-136 treatment are associated with the modulation of cell cycle and cell death pathways. Exposure to AEZS-136 resulted in sustained production of reactive oxygen species (ROS) and activation of necroptotic cell death. The necroptosis inhibitor Necrostatin-1 prevented AEZS-136-induced ROS production, mitochondrial injury, activation of JNK and cell death. Knockdown experiments identified the immediate early response 3 (IER3) as a key signaling molecule that mediates AEZS-136-resistance to oxidative death of HL cells. Furthermore, in vivo xenograft studies demonstrated a 40-70% reduction in tumor burden (P < 0.0001) and a 10-fold increase in tumor necrosis in AEZS-136-treated animals compared to control mice. These data support further clinical evaluation of AEZS-136 in refractory/relapsed HL. The Hodgkin lymphoma cell lines were obtained from the DSMZ (Braunschweig, Germany, EU). Cells were routinely maintained in RPMI medium 1640 (Lonza, Basel, Switzerland) supplemented with 20% FBS (Lonza) and 2 mM glutamine (Lonza). Cells were maintained at 37Â°C in a water-saturated atmosphere of 5% CO2 in air. 4x106 HL cells were seeded in 75 cm2 flask and, after 24 hrs, cells were treated with 10 ÂµM AEZS-136 (Aeterna Zentaris, Frankfurt, Germany, EU) in culture medium for 24 hours. At the end of treatment, cells were collected and RNA extracted.

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MicroRNA expression data from Ewing's sarcoma tumor samples

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