Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA110419 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Transcriptional analysis of genes in SKBr3 cells. Enhancer of zeste homolog 2 (EZH2) is a mammalian histone methyltransferase that contributes to the epigenetic silencing of target genes and regulates the survival and metastasis of cancer cells. EZH2 is overexpressed in aggressive solid tumors by mechanisms that remain unclear. Here we show that the expression and function of EZH2 in cancer cell lines are inhibited by microRNA-101 (miR-101).
2009-04-28 | GSE13286 | GEO
Project description:miR-101 is a tumor suppressive microRNA. Besides EZH2, a well known EZH2 target, miR-101 should have other targets, which might also contribute to its tumor suppressive function. Thus, we performed array hybridization to determine changes in gene expression upon miR-101 overexpression in U2OS cells.
2015-05-22 | GSE69150 | GEO
Project description:Background & Aims: E-cadherin expression disruption is commonly observed in epithelial cancers and metastasis. Such event is also recognized as a crucial step in gastric cancer (GC) initiation and progression. As aberrant expression of microRNAs often perturb the normal expression and function of pivotal cancer-related genes, we characterized and dissected a pathway initiated by loss of microRNA-101 that causes E-cadherin dysfunction through upregulation of EZH2 expression in GC. Methods: Microarrays were used to profile the expression of microRNAs in human GC. Array-CGH revealed DNA copy number changes that were validated by genomic quantitative PCR and Snapshot. Expression levels of microRNAs, mRNA and protein were determined by quantitative-real time PCR and western-blot/co-immunofluorescence. CDH1 inactivating mechanisms were analyzed. Gain and loss of function experiments were done in KatoIII cells. E-cadherin functionality was assessed by immunofluorescence and flow cytometry. Results: MiR-101 expression was significantly decreased in tumors in comparison with normal gastric mucosas (P<.0001). In 65% of the analyzed GC cases, miR-101 downregulation was caused by deletions and/or microdeletions at miR-101-2 locus. EZH2 overexpression and consequent loss/aberrant E-cadherin expression was found in concomitance with miR-101 downregulation in 41% of the analyzed GC cases. This occurred preferentially in cases retaining allele(s) untargeted by classical CDH1 inactivating mechanisms. MiR-101 gain of function experiments or direct inhibition of EZH2, led to a strong depletion of endogenous EZH2 protein and consequent rescue of functional E-cadherin at the cell membrane, mimicking results obtained with clinical GC samples. Conclusions: Deletions and/or microdeletions at miR-101-2 locus underlying mature miR-101 downregulation and consequent EZH2 overexpression represented a novel cascade of genetic events leading to E-cadherin disruption, preferentially affecting the intestinal-type of GC.
2012-08-01 | GSE33743 | GEO
Project description:Lack of microRNA-101 causes E-cadherin expression and function deregulation through EZH2 up-regulation in gastric cancer
| PRJNA148415 | ENA
Project description:miR-101 is a tumor suppressive microRNA. Besides EZH2, a well known EZH2 target, miR-101 should have other targets, which might also contribute to its tumor suppressive function. Thus, we performed array hybridization to determine changes in gene expression upon miR-101 overexpression in U2OS cells. U2OS were transfected with synthetic miRNA negative control (NC) or miR-101 for 48hrs, and then harvested for RNA preparation. Three independent experiments were performed. One NC sample were repeated twice for the microarray.
2015-05-22 | E-GEOD-69150 | biostudies-arrayexpress
Project description: Not available
| S-EPMC2531291 | biostudies-literature
Project description:RNA extracted at 240min. Samples are rRNA depleted. Expression measurement of Homo sapiens genes.
2019-07-31 | GSE114179 | GEO
Project description: Not available
| S-EPMC4686780 | biostudies-literature
Project description: Not available
| S-EPMC3743458 | biostudies-literature