Project description:miR-483-5p and miR-551a were over-expressed in a colon cancer cell-line LvM3b to identify genes that are down-regulated by the miRNAs over-expression. Total RNA was isolated from miR-483-5p or miR-551a over-expressing LvM3b cells as well as control LvM3b cells.
Project description:miR-483-5p and miR-551a were over-expressed in a colon cancer cell-line LvM3b to identify genes that are down-regulated by the miRNAs over-expression. Total RNA was isolated from miR-483-5p or miR-551a over-expressing LvM3b cells as well as control LvM3b cells.
Project description:miR-483-5p and miR-551a were over-expressed in a colon cancer cell-line LvM3b to identify genes that are down-regulated by the miRNAs over-expression.
Project description:miR-483-5p and miR-551a were over-expressed in a colon cancer cell-line LvM3b to identify genes that are down-regulated by the miRNAs over-expression.
Project description:To identify targets of miR-550a-3-5p in human colon cancer, HCT116 cell line expressing miR-550a-3-5p was subjected to Illumina microarrays.
Project description:miRNA abnormalities are increasingly relevent to cancer development, We used microarrays to detail the global programme of gene expression upon miR-483 overexpression in sarcoma cell line MHH-ES-1. MHH-ES-1 cells were transfected with miR-483-5p, -3p or scrambled control mimics and then harvested 48 hours after to isolate total RNAs using Trizol reagent (Invitrogen). Total RNA was converted to cRNA probes using the BioArray High Yield Transcript Labeling Kit (ENZO diagnostics), and hybridized to Affymetrix GeneChip human HG-U133ver2+ 3’-mRNA expression microarray chips using protocol EukGEs2v4 on the GeneChip Fluidic Station.
Project description:In order to identify the targets of miR-193a-5p in osteosarcoma U2OS cell line, we used a lentivirus-mediated expression system to overexpressing miR-193a precusor, miR-193a-5p target sequence and non-target sequence, respectively, in osteosarcoma cell line U2OS. A tandem mass tag (TMT)-based quantitative proteomic strategy was employed to identify the global profile of miR-193a-5p-regulated proteins. order to identify the targets of miR-193a-5p, we used a lentivirus-mediated expression system to overexpressing miR-193a precusor, miR-193a-5p target sequence and non-target sequence, respectively, in osteosarcoma cell line U2OS. A tandem mass tag (TMT)-based quantitative proteomic strategy was employed to identify the global profile of miR-193a-5p-regulated proteins.
Project description:MicroRNA-483 (miR-483) regulate endothelial function through inhibition expression of connective tissue growth factor (CTGF). Endothelial dysfunction is involved in the pathogeneis of pulmonary arterial hypertension (PAH). We investigated the role of miR-483 overexpression on human pulmonary arterial endothelial cells (hPAECs) through comparing the transcriptome file of hPAECs transfected with miR-483 -3p and -5p mimic and with control mimic. Gene ontology analysis showed that several PAH-associated signaling pathways were regulated by miR-483, including transforming growth factor-β signaling, Wnt signaling and inflammatory response, cell adhesion, response to hypoxia, apoptotic processes, oxidative reduction processes and negative regulation of cell migration and proliferation.
Project description:MiRNAs have been shown to alter both protein expression and secretion in different cellular contexts. By combining in vitro, in vivo and in silico techniques, we demonstrated that overexpression of pre-miR-1307 reduced the ability of breast cancer cells to induce endothelial cell sprouting and angiogenesis. However, the molecular mechanism behind this and the effect of the individual mature miRNAs derived from pre-miR-1307 on protein secretion and is largely unknown. Here, we overexpressed miR-1307-3p|0, -3p|1 and 5p|0 in MDA-MB-231 breast cancer cells and assessed the impact of miRNA overexpression on protein secretion by Mass Spectrometry. Unsupervised hierarchical clustering revealed a distinct phenotype induced by overexpression of miR-1307-5p|0 compared to the controls and to the 5’isomiRs derived from the 3p-arm. Together, our results suggest different impacts of miR-1307-3p and miR-1307-5p on protein secretion which is in line with our in vitro observation that miR-1307-5p, but not the isomiRs derived from the 3p-arm reduce endothelial cell sprouting in vitro. Hence these data support the hypothesis that miR-1307-5p is at least partly responsible for impaired vasculature in tumors overexpressing pre-miR-1307.
