Transcription profiling by array of castration-resistant prostate cancer PC-3 cells treated with Hsp27-siRNA or control siRNA to study the role of Heat shock protein (Hsp) 27 in splicing
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Pascal Finetti
PROVIDER: E-MTAB-1786 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:Transcriptional profiling of HPMECs comparing Control siRNA treated with HSP27 siRNA Two-condition experiment, control siRNA vs HSP27 siRNA ; 3 controlsiRNA transfected replicates , 3HSP27 siRNA replicates. Replicates were pooled and hybridized to a single array.
2015-08-29 | E-GEOD-72485 | biostudies-arrayexpress
Project description:Transcriptional profiling of HPMECs comparing Control siRNA treated with HSP27 siRNA
2015-08-29 | GSE72485 | GEO
Project description:SMILE, a molecule for which no information is available in the literature, is overexpressed in the blood of patients tolerating a kidney graft without treatment. We performed microarray analysis to determine cellular functions affected by SMILE silencing. Each condition of control and SMILE siRNA transfected cells was made in triplicates.
2010-05-27 | E-GEOD-21886 | biostudies-arrayexpress
Project description:To get insight in the functional role of EGR2 for Ewing sarcoma, we performed a transcriptional profiling of Ewing sarcoma cells after knockdown of EGR2 and compared the resulting transcriptional signature with that of EWSR1-FLI1-silenced Ewing sarcoma cells. In accordance with the strong EGR2-induction by EWSR1-FLI1, both genes highly significantly overlap in their transcriptional signatures. Gene-set enrichment analyses (GSEA) and DAVID (Database for Annotation, Visualisation and Integrated Discovery) gene ontology analyses indicated a strong impact of EGR2 on cholesterol and lipid biosynthesis resembling its function in orchestrating lipid metabolism of myelinating Schwann cells. A673 and SK-N-MC Ewing sarcoma cells were transfected with specific siRNAs directed against EGR2 or EWSR1-FLI1 or non-targeting control siRNA. 48 h thereafter RNA was harvested and processed for microarray analysis.
2015-07-26 | E-GEOD-62090 | biostudies-arrayexpress
Project description:The aim of the present study was to investigate the potential role of HIF-2a in regulating RCC susceptibility to natural killer (NK) cell-mediated killing. We demonstrated that the RCC cell line 786-O with mutated VHL was resistant to NK-mediated lysis as compared to the VHL corrected cell line (WT7). This resistance was independent of immunological synapse formation and NK ligand expression but was found to be reliant on HIF-2a stabilization in 786-0 cells. In order to elucidate the molecular basis of HIF-2a-induced impairment of NK-mediated killing, we performed global gene analysis using DNA microarray. Three candidate genes (ANGPTL4, ADM and ITPR1) were selected on the basis of their fold change and their involvement in cell death and survival. SiRNA targeting of these genes revealed that only ITPR1 silencing resulted in a significant increase of 786-O susceptibility to NK-mediated lysis. Using gene silencing of HIF2-a and chromatin immunoprecipitation assay, we showed for the first time that ITPR1 was a direct novel target of HIF2-a. Notably, a strong and significant correlation was found between ITPR1and HIF2-a staining in RCC patients. Transcriptional profiling of ITPR1silenced RCC cells indicated that several important genes involved in cell survival and apoptosis were differentially regulated. Using ITPR1 silenced Renca cells, we further found that ITPR1 was involved in the control of tumor progression. Moreover ITPR1 targeting combined with NK depletion significantly enhanced tumor growth as compared to ITPR1 knocked down Renca xenografts. Our data provide insights into the link between HIF-2a, ITPR1-related pathway and natural immunity and suggest a role of the HIF2/ITPR1 axis in regulating RCC cell survival.
2014-01-11 | E-MTAB-1802 | biostudies-arrayexpress
Project description:A "Cartes d'Identite des Tumeurs" (CIT) project from the french Ligue Nationale Contre le Cancer (http://cit.ligue-cancer.net). Affymetrix UU133A gene expression data for a series of 32 cases of systemic Anaplastic Large Cell Lymphoma<br> (ALCL) and 5 ALCL cell lines; used to (1) confirm that tumors expressing Anaplastic Lymphoma Kinase (ALK+ ALCL) and ALK- ALCLs are different entities, (2) identify most significantly differentially expressed genes between ALK+ and ALK- samples, (3) generate a molecular signature of ALK- ALCL, (4) perform unsupervised analysis classifying ALCL in sub-groups related to morphology and clinical variables (e.g. disease stage and enrichment with 'early relapse' patients).<br> <br> Principal Investigator: Dr Georges DELSOL-- Centre de Physiopathologie Toulouse-Purpan CHU-Purpan -- Toulouse -- France -- Email: delsol.g@chu-toulouse.fr <br> Programme "Cartes d'identite des Tumeurs" (CIT) of the "Ligue Nationale Contre le Cancer" (LNCC)<br> Submitter: Fabien PETEL (petelf@ligue-cancer.net)
2007-05-05 | E-TABM-117 | biostudies-arrayexpress
Project description:human bronchial smooth muscle cells were infected with adenoviral constructs containing either the phosphorylation mutant form of HSP27 (HSP27-3A) or the wild type form (HSP27-WT) at 40 MOI for 4 days. All sets were stimulated with a cytokine mixture containing 10 ng/ml IL-1beta, TNF-alfa, and gamma-IFN for 20 hours prior to harvest. This series represents 4 separate preparations of cells and RNA, with each set being subjected to a dye flip and hybridized to 2 different slides. Keywords: parallel sample
2004-04-09 | GSE1292 | GEO
Project description:In neuroblastoma (NB), the presence of segmental chromosome alterations (SCA) is associated with a higher risk of relapse, even when occurring together with numerical chromosome alterations (NCA). Furthermore, recent evidence shows that SCAs play a role in tumor progression. In order to analyze the role of SCAs in infants with NB, we have performed an extensive retrospective array-CGH analysis of tumours from infants enrolled in the European INES 99.1, 99.2 and 99.3 trials. Tumour samples from 221/300 enrolled patients could be analyzed. SCAs were observed in 11%, 20% and 59% of infants enrolled in trial 99.1 (localised unresectable NB), 99.2 (INSS stage 4s) and 99.3 (INSS stage 4), respectively (p<0.001), and were associated with the presence of bone metastasis (p<0.003). Progression-free survival was poorer in patients whose tumours harbored at least one SCA, in the whole population as well as in trials 99.1 and 99.2. In multivariate analysis, taking into account single genetic alterations, the protocol arm and genomic profile, the SCA genomic profile was the strongest predictor of poor outcome. Although overall survival was excellent, patients with stage 4s disease and a SCA genomic profile had a higher risk of relapse also in the absence of clinical symptoms at diagnosis and required a higher treatment burden for salvage. In conclusion, in infants with NB, a SCA genomic profile is useful to identify patients who will require upfront treatment even in the absence of other clinical indication for therapy, whereas an NCA genomic profile can identify a patient subpopulation in whom treatment reduction can be considered safe. Each of the 218 tumoral genomic DNAs was hybridized against non-tumoral DNA reference on BAC/PAC array or commercial supports in order to determine an overall genomic profile. The reference DNA was obtained from the blood of a single normal individual.
2011-12-07 | E-GEOD-26494 | biostudies-arrayexpress
Project description:human bronchial smooth muscle cells were infected with adenoviral constructs containing either the phosphorylation mutant form of HSP27 (HSP27-3A) or the wild type form (HSP27-WT) at 40 MOI for 4 days. All sets were stimulated with a cytokine mixture containing 10 ng/ml IL-1beta, TNF-alfa, and gamma-IFN for 20 hours prior to harvest. This series represents 4 separate preparations of cells and RNA, with each set being subjected to a dye flip and hybridized to 2 different slides.
2010-06-09 | E-GEOD-1292 | biostudies-arrayexpress
Project description:Abstract: Purpose: To identify a DNA signature to predict metastasis of small node-negative breast carcinoma Experimental Design: The authors used Comparative Genomic Hybridization (CGH) array to analyze 168 pT1T2pN0 invasive ductal carcinoma patients with either good (no event 5 years after diagnosis: 111 patients) or poor (57 patients with early onset metastasis) outcome. A CGH classifier, identifying low and high-risk groups of metastatic recurrence, was established in a training set of 78 patients. This classifier was based on both genomic regions with statistically different alterations between the two groups of clinical outcome and the number of alterations. It was then tested on a validation set of 90 patients and compared to clinicopathological parameters. Results: The genomic status of regions located on chromosomes 2p22.2, 3p23 and 8q21-24 and the number of segmental alterations were defined in the training set to classify tumors into low or high-risk groups. In the validation set, this CGH classifier produced a highly significant odds ratio of 10.39 (95%CI: 3.75-28.78, p=6.63Ã10-6, Wald test) in univariate analysis with a sensitivity of 66%, a specificity of 84% and an accuracy rate of 78%. The 5-year metastasis-free survival analysis showed a highly significant difference between the two predicted groups (Hazard Ratio=5.7, p=1.82Ã10-7, log-rank test). Together with estrogen receptor and grade, this CGH classifier provided significant prognostic information in multivariate analysis. Conclusions: In addition to classical parameters, this DNA signature may constitute an accurate tool to identify patients with T1T2N0 luminal tumors, who may benefit from adjuvant treatments. Each of the 168 tumoral genomic DNA was hybridized against the same non tumoral DNA reference following identical protocol
2010-05-19 | E-GEOD-19159 | biostudies-arrayexpress