Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA340166 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Impaired skeletal muscle function is a central feature in the pathophysiology of type 2 diabetes (T2DM). The disease phenotype could be due to immature muscle cell development, which in turn may occur as the result of disturbed microRNA-mediated regulation of muscle differentiation in T2DM. To address this hypothesis, we assessed global miRNA expression during in vitro differentiation of muscle stem cells derived from T2DM patients and healthy controls. We identified the mir-23b/27b cluster to be downregulated in the patients, and further demonstrated that a pro-myogenic effect of these miRNAs occurs through targeting of several genes in the p53 pathway, which was concordantly dysregulated in the muscle cells derived from humans with T2DM. In conclusion, we have identified a novel myogenesis-controlling pathway, the miR-23b/27b-p53 axis, potentially contributing to the sustained multiple muscular dysfunctions in T2DM in humans.
2017-08-12 | GSE86069 | GEO
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.
2016-02-10 | E-GEOD-76620 | biostudies-arrayexpress
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.
2016-02-10 | GSE76620 | GEO
Project description:Transcriptional profiling of 4TO7 cells featuring ectopic expression of miR-23b/27b/24 compared to vector control cells. Gene expression changes will be examined as potential direct targets of the miRNAs for use in later studies on metastasis suppression or activation.
2014-12-23 | GSE57838 | GEO
Project description:4TO7 cells: miR-23b/27b/24 overexpression vs control
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Project description:MiR-23b/-27b Targets in Prostate Cancer Cell Lines
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Project description:To identify differentially expressed genes by anti cancer treatments (microRNAs, siRNAs and chemical compounds) in human cancer, several cell lines (prostate cancer, renal cell carcinoma and head and neck squamous cell carcinoma) were subjected to Agilent whole genome microarrays. Human cancer cell lines (PC3, DU145, LNCap, A498, 786-O, FaDu and SAS) were treated with miRNAs (miR-145, miR-375, miR-23b, miR-24, miR-27b and miR-29a), siRNAs (si-CAV2, si-LAMB3 and si-GOLM1) and chemical compunds (genistein, wogonin and CXCL10).
2013-09-25 | E-GEOD-47657 | biostudies-arrayexpress
Project description:Transcriptional profiling of 4TO7 cells featuring ectopic expression of miR-23b/27b/24 compared to vector control cells. Gene expression changes will be examined as potential direct targets of the miRNAs for use in later studies on metastasis suppression or activation. Two-condition experiment, miRNA overexpressing cells vs vector control. Biological replicates: 2 transfection replicates each.
2014-12-23 | E-GEOD-57838 | biostudies-arrayexpress
Project description:Aged skeletal muscle is markedly affected by fatty muscle infiltration and strategies to reduce the occurrence of adipocytes within skeletal muscle, the intramuscular adipose tissue (IMAT), are urgently needed. Fibroblast growth factor-2 (FGF-2) is a critical growth factor for muscle tissue. Here, we show that FGF-2 not only stimulates muscle growth, but also promotes intramuscular adipogenesis. Using multiple screening assays for upstream and downstream signaling of microRNA (miR)-29a we located the secreted protein and adipogenic inhibitor SPARC to an FGF-2 signaling pathway that is conserved between skeletal muscle cells from mice and humans and that is activated in skeletal muscle from aged mice. FGF-2 induces the miR-29a/SPARC axis through transcriptional activation of FRA-1 which binds and activates an evolutionary conserved AP-1 site element proximal in the miR-29a promoter. Genetic deletions in muscle cells and AAV-mediated overexpression of FGF-2 or SPARC in mouse skeletal muscle revealed that this axis regulates differentiation of fibro/adipogenic progenitors in vitro and intramuscular fat formation in vivo. Thus, our data highlight an ambivalent role of FGF-2 for adult skeletal muscle and reveal a novel pathway to combat fat accumulation in aged skeletal muscle.
2021-08-23 | PXD020575 | Pride
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).
2015-06-18 | GSE67631 | GEO