Project description:We report the application of transcriptome sequencing for investigating of the hsa-miR-371a-5p and hsa-miR-518a-3p regulated genes. JAR, JEG-3 and BeWo choriocarcinoma cells were transfected with hsa-miR-371a-5p or hsa-miR-518a-3p inhibitors or control inhibitors. Totally, 237, 132 and 277 genes with > 2 folds change and adjusted P < 0.05 were upregulated in JAR, JEG-3 and BeWo cells respectively after hsa-miR-371a-5p knockdown. Meanwhile, 229, 269 and 191 genes were upregulated in JAR, JEG-3 and BeWo cells respectively after hsa-miR-518a-3p knockdown. The top upregulated genes included many oncogenes or oncogenesis associated ones. Enrichment analysis showed hsa-miR-371a-5p and hsa-miR-518a-3p regulated diverse pathways related to tumorigenesis and metastasis. Our results would be helpful for the searching of early molecular biomarkers and therapeutic targets for gestational trophoblastic neoplasia.
Project description:We analyzed the expression profiles of hsa-miR-145-5p or hsa-miR-31-5p-targeting genes relating to invasion or migration after co-overexpression of hsa-miR-145-5p and 31-5p Gene expression profiles of U87 cells after co-transfection with hsa-miR-145-5p and 31-5p mimics, and U87 cells after transfection miR mimic negative control
Project description:Total RNA samples from three biological replicates in which the hsa-mir-98 was overexpressed in HeLa cells were profiled by gene expression. As negative control, we used total RNA samples from HeLa cells transfected with cel-mir-67 Keywords: gene expression array-based (RNA / in situ oligonucleotide)
Project description:Total RNA samples from three biological replicates in which the hsa-mir-26b was overexpressed in HeLa cells were profiled by gene expression. As negative control, we used total RNA samples from HeLa cells transfected with cel-mir-67 Keywords: gene expression array-based (RNA / in situ oligonucleotide)
Project description:Primary Myelofibrosis (PMF) is a myeloproliferative neoplasm characterized by hyperplastic megakaryopoiesis and myelofibrosis. Through a gene expression profile (GEP) study we recently highlighted the upregulationof miR-34a-5p in PMF versus healthy donor (HD) CD34+ hematopoietic progenitor cells (HPCs). To shed some light into the role of miR-34a-5p in PMF pathogenesis, here we unravelled the effects of the overexpression of miR-34a-5p in HPCs forcing its expression in HPCs. We showed that enforced expression of miR-34a-5p blocks proliferation and favours the megakaryocyte and monocyte/macrophage commitment of HPCs. Interestingly, we identified lymphoid enhancer-binding factor 1 (LEF1) and nuclear receptor subfamily 4, group A, member 2 (NR4A2) transcripts as miR-34a-5p-targets downregulated after miR-34a-5p overexpression in HPCs as well as in PMF compared with HD HPCs. Remarkably, the knockdown of NR4A2 in HPCs mimicked the antiproliferative effects of miR-34a-5p overexpression, while the silencing of LEF1 phenocopied the effects of miR-34a-5p overexpression in HPCs lineage choice, by stimulating the megakaryocyte and monocyte/macrophage commitment.
Project description:The aim of this small RNA Seq is to determine if the sequence reads observed for hsa-miR-34b-5p and hsa-miR-449c-5p represent library artifacts or sequencing artifacts
Project description:We have employed whole genome microarray to identify changes in gene expression in MDA-MB-231 cells transfected with hsa-miR-205-5p and hsa-miR-214-3p compared to scrambled miRNA precursors at 72 hours after transfection.
Project description:Myocardial regeneration is restricted to early postnatal life, when mammalian cardiomyocytes still retain the ability to proliferate. The molecular cues that induce cell cycle arrest of neonatal cardiomyocytes towards terminally differentiated adult heart muscle cells remain obscure. We report that the miR-106b~25cluster is higher expressed in the early postnatal myocardium and decreases in expression towards adulthood, especially under conditions of overload, and orchestrates the transition of cardiomyocyte hyperplasia towards cell cycle arrest and hypertrophy by virtue of its targetome. To identify the relevant targets of individual miRNAs in the miR-106b~15 cluster and elucidate the molecular mechanisms underlying the proliferative effects of this microRNA cluster, we assessed the global transcriptomic changes by deep-sequencing total neonatal mouse cardiomyocyte RNA after exogeneous transfection with hsa-miR-106b-5p, hsa-miR-93-5p, hsa-miR-25-3p and compared the transcriptomic profiles to cardiomyocytes transfected with cel-miR-67, a control miRNA.
Project description:Total RNA samples from three biological replicates in which the hsa-mir-98 was overexpressed in HeLa cells were profiled by gene expression. As negative control, we used total RNA samples from HeLa cells transfected with cel-mir-67 Experiment Overall Design: hsa-miR-98 transfection
Project description:Total RNA samples from three biological replicates in which the hsa-mir-26b was overexpressed in HeLa cells were profiled by gene expression. As negative control, we used total RNA samples from HeLa cells transfected with cel-mir-67 Experiment Overall Design: hsa-miR-26b transfection