Project description:In this experiment, we want to assess the effect of a lentiviral miR-10a and miR-335 overexpression on the transcriptome of murine LSK (Lin-,Sca-1+,c-Kit+) cells. Primary LSK cells were transduced with lentiviral miRNA overexpression constructs (control: GFP overexpression) and sorted for transduced cells (GFP+) after five days of in vitro culture (Flt-3, TPO, IL-3, SCF containing media).
Project description:To clarify the effect of miRNAs, we carried out a gene expression microarray analysis using GIST-T1 cells transfected with a miR-335 mimic or a negative control. We found that 1,095 probe sets (853 unique genes) were downregulated (>1.5-fold) by ectopic miR-335 expression.
Project description:To clarify the effect of miRNAs, we carried out a gene expression microarray analysis using GIST-T1 cells transfected with a miR-335 mimic or a negative control. We found that 1,095 probe sets (853 unique genes) were downregulated (>1.5-fold) by ectopic miR-335 expression. GIST-T1 cells were transfected with a mirVana miR-335 mimic (Ambion) or a mirVana miRNA mimic Negative Control #1 (Ambion). Forty-eight hours after transfection, total RNA extraction was carried out, and gene expression signatures were analyzed.
Project description:the LM2 breast cancer cell line is an in vivo derived line from the MDA-MB-231 parental line. this LM2 line has been transduced either with a short hairpin control or miR-335 expression vector. Experiment Overall Design: the LM2 cell line is transduced either with a short hairpin control vector or miR-335 expression vector.
Project description:the LM2 breast cancer cell line is an in vivo derived line from the MDA-MB-231 parental line. this LM2 line has been transduced either with a short hairpin control or miR-335 expression vector. Keywords: breast cancer, metastasis, miRNA
Project description:Human mesenchymal stem cells (hMSC) have an extensive potential for clinical applications in cell therapy. However, very little is known of the specific molecular regulatory mechanisms that control the therapeutical properties of these cells. We aimed to identify microRNAs (miRNAs) that could be involved in controlling the transition between the self-renewing (undifferentiated) and the reparative (differentiated) phenotypes of hMSCs. MicroRNA microarrays were used to identify miRNAs that are upregulated in undifferentiated hMSCs. For that, we compared the miRNA expression profiles of undifferentiated bone marrow-derived hMSCs with the same primary cell lines after 9 days of in vitro adipogenic or osteogenic induction. We also compared the miRNA expression profiles of undifferentiated hMSCs with skin fibroblasts (a mesenchymal cell lineage with a more restricted differentiation potential). These experiments allowed us to identify miR-335 as the only miRNA downregulated upon MSC differentiation as well as in MSCs in comparison with skin fibroblasts. Gene expression microarrays were used to identify genes that are downregulated in hMSCs overexpressing miR-335. We compared the miRNA expression profiles of hMSCs transduced with a lentiviral vector encoding miR-335 with MSCs transduced with a control lentiviral vector. Our results suggest miR-335 downregulation could be a critical trigger for the initiation of MSCs activities involved in tissue repair and remodelling, including cell proliferation, migration and differentiation.