Project description:To claryfy the genes regulated by miR-27b in human hepatic cells, whole human genome microarrays were employed to analyze gene expression.
Project description:Analysis of genes regulated by miR-23b/-27b overexpression in aggressive PC3-ML cells, confirmed by antagomiR inhibition of miR-23b and miR-27b in the relatively indolent cell line LNCaP. Genes that were downregulated in PC3-ML overexpression and upregulated with LNCaP inhibition were further explored as downstream targets of miR-23b/-27b.
Project description:Analysis of genes regulated by miR-23b/-27b overexpression in aggressive PC3-ML cells, confirmed by antagomiR inhibition of miR-23b and miR-27b in the relatively indolent cell line LNCaP. Genes that were downregulated in PC3-ML overexpression and upregulated with LNCaP inhibition were further explored as downstream targets of miR-23b/-27b. PC3-Ml cells were transduced with miR-23b/-27b or a scrambled miRNA control, and only cells expressing greater than 95% transduction efficiency were used for array. LNCaP cells were transfected with antagomiRs to miR-23b and miR-27b, or a non-coding control.
Project description:To understand the effect of reducing miR-27b levels on genome-wide expression in cortical neurons and identify potential targets of miR-27b, we generated dissociated cortical neuron cultures and treated them with lentivirus to knock down miR-27b.
Project description:To understand the effect of reducing miR-27b levels on genome-wide expression in cortical neurons and identify potential targets of miR-27b, we generated dissociated cortical neuron cultures and treated them with lentivirus to knock down miR-27b. 2 treatment conditions (control lentivirus or lentivirus to knock down miR-27b); 3 neuronal preparations of dissociated mouse cortical neurons; total of 6 samples
Project description:Drug resistance, caused by complex and redundant mechanisms, is a major obstacle in cancer treatment, especially in liver and kidney cancers. Combinational therapy of miRNAs, which concurrently target multiple pathways, with anticancer drugs represent a new strategy to improve the drug response. By a systems approach, we identified that miR-27b, a miRNA deleted in liver and kidney cancers, sensitizes cancer cells to a broad spectrum of anticancer drugs in vitro and in vivo. Two samples transfected with nontarget miRNA control or miR-27b mimics followed by 48 hours doxorubicin treatment
Project description:In our previous study, hsa-let-7d-5p,hsa-miR-27b-3p,hsa-miR-151-5p were significantly upregulated in the plasma of atopic patients. To study the each function of hsa-let-7d-5p,hsa-miR-27b-3p,hsa-miR-151-5p, which are significantly upregulated in the plasma of atopic patients, we performed mimic-transfected THP-1 cells, a mononuclear cell line, and performed comprehensive genetic analysis.
Project description:Aim: The heart undergoes pathological remodelling under increased stress and neuronal imbalance. MicroRNAs (miRNAs) are involved in post-transcriptional regulation of genes in cardiac physiology and pathology. However, the mechanisms underlying miRNA-mediated regulation of pathological cardiac remodelling remain to be studied. This study aims to explore the function of endogenous microRNA-27b-3p (miR-27b-3p) in pathological cardiac remodelling. Methods and results: We found that miR-27b-3p expression was elevated in heart of patients with cardiac hypertrophy and in transverse aortic constriction (TAC)-induced cardiac hypertrophy mouse model. MiR-27b-3p-knockout mice showed significantly attenuated cardiac hypertrophy, fibrosis, and inflammation induced by two independent pathological cardiac hypertrophy models, TAC and Angiotensin II (Ang II) perfusion. Transcriptome sequencing analysis revealed that miR-27b-3p deletion significantly downregulated TAC-induced cardiac hypertrophy, fibrosis, and inflammatory genes. We identified fibroblast growth factor 1 (FGF1) as a novel miR-27b-3p target gene in the heart, which was upregulated in miR-27b-3p-null mice. Conclusions: Our study has demonstrated that miR-27b-3p induces pathological cardiac remodelling and suggests that inhibition of endogenous miR-27b-3p or administration of FGF1 might have the potential to suppress cardiac remodelling in a clinical setting.
Project description:To identify the microRNA-27b (miR-27b) target genes in luminal-type breast cancer cells, we performed the microarray analysis using miR-27b knockdown MCF7-luc cell line (MCF7-luc anti-miR-27b), miR-27b overexpressing MCF7-luc cell line (MCF7-luc miR-27b o.e.) and their contro cell line (MCF7-luc anti-NC).
Project description:To identify the microRNA-27b (miR-27b) target genes in luminal-type breast cancer cells, we performed the microarray analysis using miR-27b knockdown MCF7-luc cell line (MCF7-luc anti-miR-27b), miR-27b overexpressing MCF7-luc cell line (MCF7-luc miR-27b o.e.) and their contro cell line (MCF7-luc anti-NC). After establishing MCF7-luc anti-miR-27b, MCF7-luc miR-27b o.e. and MCF7-luc anti-NC using lentivirus vector, we performed the microarray analysis.