Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA184876 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Analysis of the effect of the miRNA set (miR-32/455/181a/181b) on global gene expression. The hypothesis tested was that overexpression of these miRNAs would produce changes in gene expression similar to changes caused by PI3K knockdown. Data provided insight into genes that are disrupted with either individual miRNA and siRNA or the combination of miRNAs or siRNAs. Total RNA was isolated from KYSE30 cells transfected with either miRNA or siRNA for global expression analysis.
2012-12-29 | E-GEOD-43195 | biostudies-arrayexpress
Project description:Analysis of the effect of the miRNA set (miR-32/455/181a/181b) on global gene expression. The hypothesis tested was that overexpression of these miRNAs would produce changes in gene expression similar to changes caused by PI3K knockdown. Data provided insight into genes that are disrupted with either individual miRNA and siRNA or the combination of miRNAs or siRNAs.
2012-12-29 | GSE43195 | GEO
Project description:Long non-coding RNAs (lncRNAs) play pivotal roles in diseases such as osteoarthritis (OA). However, knowledge of the biological roles of lncRNAs is limited in OA. We aimed to explore the biological function and molecular mechanism of HOTTIP in chondrogenesis and cartilage degradation. We used the human mesenchymal stem cell (MSC) model of chondrogenesis, in parallel with, tissue biopsies from normal and OA cartilage to detect HOTTIP, CCL3, and miR-455-3p expression in vitro. Biological interactions between HOTTIP and miR-455-3p were determined by RNA silencing and overexpression in vitro. We evaluated the effect of HOTTIP on chondrogenesis and degeneration, and its regulation of miR-455-3p via competing endogenous RNA (ceRNA). Our in vitro ceRNA findings were further confirmed within animal models in vivo. Mechanisms of ceRNAs were determined by bioinformatic analysis, a luciferase reporter system, RNA pull-down, and RNA immunoprecipitation (RIP) assays. We found reduced miR-455-3p expression and significantly upregulated lncRNA HOTTIP and CCL3 expression in OA cartilage tissues and chondrocytes. The expression of HOTTIP and CCL3 was increased in chondrocytes treated with interleukin-1β (IL-1β) in vitro. Knockdown of HOTTIP promoted cartilage-specific gene expression and suppressed CCL3. Conversely, HOTTIP overexpression reduced cartilage-specific genes and increased CCL3. Notably, HOTTIP negatively regulated miR-455-3p and increased CCL3 levels in human primary chondrocytes. Mechanistic investigations indicated that HOTTIP functioned as ceRNA for miR-455-3p enhanced CCL3 expression. Taken together, the ceRNA regulatory network of HOTTIP/miR-455-3p/CCL3 plays a critical role in OA pathogenesis and suggests HOTTIP is a potential target in OA therapy.
2019-08-12 | PXD014988 | Pride
Project description:The molecular mechanism responsible for Ewing Sarcoma (ES) remains largely unknown. This study compared global miRNA expression in biopsies from 20 ES patients, affected by primary untreated tumors, with miRNA expressed in normal human mesenchymal stromal cells (MSCs) by microarray analysis. A miRTarBase database was used to identify the predicted target genes for differentially-expressed miRNAs. The miRNAs microarray analysis revealed distinct patterns of miRNA expression between ES biopsies and normal MSCs. 58 of the 954 analyzed miRNAs were significantly differentially expressed in ES samples compared to MSCs. Moreover, the qRT-PCR analysis, carried out on three selected miRNAs, showed that miR-181b, miR-1915 and miR-1275 were significantly aberrantly-regulated, confirming the microarray results. Bio-database analysis identified BCL-2 as a bona fide target gene of the miR-21, miR-181a, miR-181b, miR-29a, miR-29b, miR-497, miR-195, miR-Let-7a, miR-34a. Using paraffin-embedded tissues from ES, this study has identified several potential target miRNAs and one gene that might be considered novel critical biomarkers for ES pathogenesis.
2016-12-26 | GSE80201 | GEO
Project description:Overexpression of miR-181a in AML blasts: DNA Microarray was performed to compare overall gene expression profiles of KG-1 Anti-miR-CT and U937 Anti-miR-CT cells compared respectively to KG-1 Anti-miR-181a and U937 Anti-miR-181a.
2014-12-30 | E-MTAB-2837 | biostudies-arrayexpress
Project description:MicroRNAs are short non-coding RNA molecules playing regulatory roles in animals and plants by repressing translation or cleaving RNA transcripts. The specific modulation of several microRNAs has been recently associated to some forms of human cancer, suggesting that these short molecules can represent a new class of genes involved in oncogenesis. In our study, we examined by microarray the global expression levels of 245 microRNAs in glioblastoma multiforme (GBM), the most frequent and malignant of primary brain tumors. The analysis of both glioblastoma tissues and glioblastoma cell lines allowed us to identify a group of microRNAs whose expression is significantly altered in this tumor. The most interesting results came from miR-221, strongly upregulated in glioblastoma and a set of brain-enriched miRNAs, miR-128, miR-181a, miR-181b, miR-181c, which are down-regulated in glioblastoma.
2005-09-23 | E-TABM-37 | biostudies-arrayexpress
Project description:Molecular subtypes of SCLC have been defined by the expression status of ASCL1, NEUROD1, YAP1, and POU2F3 transcription regulators. ASCL1 knockdown resulted in decreased and increased expression of miR-375 and miR-455-3p, respectively. Analyses of publicly available transcriptome datasets suggested that miR-375 induced by ASCL1 is involved in YAP1 suppression whereas miR-455-3p is higher in non-neuroendocrine SCLC cells lacking ASCL1 expression.
2021-07-25 | GSE180315 | GEO
Project description:Molecular subtypes of SCLC have been defined by the expression status of ASCL1, NEUROD1, YAP1, and POU2F3 transcription regulators. ASCL1 knockdown resulted in decreased and increased expression of miR-375 and miR-455-3p, respectively. Analyses of publicly available transcriptome datasets suggested that miR-375 induced by ASCL1 is involved in YAP1 suppression whereas miR-455-3p is higher in non-neuroendocrine SCLC cells lacking ASCL1 expression.
2021-07-25 | GSE180314 | GEO
Project description:Increased expression levels of miR-181 family members have been shown to be associated with favorable outcome in patients with cytogenetically normal acute myeloid leukemia. Here we show that increased expression of miR-181a and miR-181b is also significantly (P < .05; Cox regression) associated with favorable overall survival in cytogenetically abnormal AML (CA-AML) patients. We further show that up-regulation of a gene signature composed of 4 potential miR-181 targets (including HOXA7, HOXA9, HOXA11, and PBX3), associated with down-regulation of miR-181 family members, is an independent predictor of adverse overall survival on multivariable testing in analysis of 183 CA-AML patients. The independent prognostic impact of this 4-homeobox-gene signature was confirmed in a validation set of 271 CA-AML patients. Furthermore, our in vitro and in vivo studies indicated that ectopic expression of miR-181b significantly promoted apoptosis and inhibited viability/proliferation of leukemic cells and delayed leukemogenesis; such effects could be reversed by forced expression of PBX3. Thus, the up-regulation of the 4 homeobox genes resulting from the down-regulation of miR-181 family members probably contribute to the poor prognosis of patients with nonfavorable CA-AML. Restoring expression of miR-181b and/or targeting the HOXA/PBX3 pathways may provide new strategies to improve survival substantially. In addition, this data set has been used to identify a common prognostic gene signature (Li Z. et al. unpublished). 65 human AML samples bearing various cytogenetic and molecular abnormalities are used to identify miR-181 target genes and a common prognostic gene signature.
2012-04-03 | E-GEOD-30258 | biostudies-arrayexpress
Project description:Increased expression levels of miR-181 family members have been shown to be associated with favorable outcome in patients with cytogenetically normal acute myeloid leukemia. Here we show that increased expression of miR-181a and miR-181b is also significantly (P < .05; Cox regression) associated with favorable overall survival in cytogenetically abnormal AML (CA-AML) patients. We further show that up-regulation of a gene signature composed of 4 potential miR-181 targets (including HOXA7, HOXA9, HOXA11, and PBX3), associated with down-regulation of miR-181 family members, is an independent predictor of adverse overall survival on multivariable testing in analysis of 183 CA-AML patients. The independent prognostic impact of this 4-homeobox-gene signature was confirmed in a validation set of 271 CA-AML patients. Furthermore, our in vitro and in vivo studies indicated that ectopic expression of miR-181b significantly promoted apoptosis and inhibited viability/proliferation of leukemic cells and delayed leukemogenesis; such effects could be reversed by forced expression of PBX3. Thus, the up-regulation of the 4 homeobox genes resulting from the down-regulation of miR-181 family members probably contribute to the poor prognosis of patients with nonfavorable CA-AML. Restoring expression of miR-181b and/or targeting the HOXA/PBX3 pathways may provide new strategies to improve survival substantially. In addition, this data set has also been used to identify a common prognostic gene signature in human AML (Li Z. et al., unpublished). 93 human AML samples bearing various cytogenetic and molecular abnormalities are used to identify miR-181 target genes and a common prognostic gene signature.
2012-04-03 | E-GEOD-30285 | biostudies-arrayexpress