Dysregulated miRNA expression is observed in PKD, but whether miRNAs are directly involved in kidney cyst formation and growth is not known. Here,we show that miR-17~92, an oncogenic miRNA cluster, is up-regulated in mouse models of PKD. Kidney-specific transgenic overexpression of miR-17~92 produces kidney cysts in mice.

Results We found the miR-17-92 cluster to be downregulated in chemoresistant CSCs versus non-CSCs and demonstrate its crucial relevance for CSC biology. In

Although miR-17-92 cluster are located at 13q31.3, the expression of miR-18, miR-19 and miR-20 (especially miR-19) in patients with del (13q14) was higher than those without del (13q14). Patients with miR-17, miR-20 and miR-92 high-expression had shorter PFS compared to those with miR-17, miR-20 and miR-92 low-expression. MicroRNA-17-92 (miRNA-17-92 or miR-17-92) is a miRNA cluster that regulates cell growth and immunity, but the role of miR-17-92 cluster in keratinocytes and its relation to skin diseases have not been well investigated. miR-17~92 miRNA cluster promotes kidney cyst growth in polycystic kidney disease.

Mirna 17-92 cluster

studied the function of the miR-17~92 cluster and its paralogs miR-106a~363 and miR-106b~25 by generating mice deficient for each of these miRNA clusters.14 While The miR-17-92 cluster (encoding miR-17, -18a, -19a/b, -20a, and miR-92a) is highly expressed in tumor cells and is up-regulated by ischemia. Whereas miR-92a was recently identified as negative regulator of angiogenesis, the specific functions of the other members of the cluster are less clear. miR-17∼92 miRNA Cluster Is Up-Regulated in Mouse Models of PKD. To identify miRNAs that are differentially expressed between cystic kidneys and normal kidneys, we performed miRNA microarrays using RNA from kidneys of control and kidney-specific-cadherin (Ksp)/cre;Kif3a F/F (Kif3a-KO) mice, an animal model of PKD. Many RNAs are processed into biologically active transcripts, the aberrant expression of which can contribute to disease phenotypes. For example, the primary microRNA-17-92 (pri-miR-17-92) cluster contains six microRNAs (miRNAs) that collectively act in several disease settings. The miRNA-17 ∼ 92 cluster mediates chemoresistance and enhances tumor growth in mantle cell lymphoma via PI3K/AKT pathway activation. Leukemia 26, 1064–1072 (2012).

MicroRNA (miRNA)-17-92 cluster (miR-17-92), containing seven individual miRNAs, is frequently amplified and overexpressed in lymphomas and various solid tumors. We have found that it is also frequently amplified and the miRNAs are aberrantly overexpressed in mixed lineage leukemia (MLL)-rearranged acute leukemias.

2010-08-01 · One of the best-characterized oncogenic miRNAs is mir-17-92, a polycistronic miRNA cluster also designated as oncomir-1 (He et al., 2005).The precursor transcript derived from the mir-17-92 gene contains six tandem stem-loop hairpin structures that ultimately yield six mature miRNAs: miR-17, miR-18a, miR-19a, miR-20a, miR-19b-1, and miR-92-1 (Tanzer and Stadler, 2004). 3. Expression and regulation of the miRNA-17-92 cluster in tumor cells Expression and functions of miR-17/20a.

MiR-17-92, a highly conserved gene cluster, has 6 members including miR-17, miR-18a, miR-19a, miR-20a, miR-19b-1 and miR-92a. The miR-17-92 cluster,

Forskningsoutput: Tidskriftsbidrag › Artikel i The miR-17-92 MicroRNA Cluster Regulates Multiple Components of the TGF-beta Pathway in Neuroblastoma.

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Usually, miRNA clusters consist of two or three miRNAs, but larger clusters also exist, for example, the miR-17-92 cluster is found on human chromosome 13 and is composed of six miRNAs. miRNA miR-17∼92 miRNA Cluster Is Up-Regulated in Mouse Models of PKD. To identify miRNAs that are differentially expressed between cystic kidneys and normal kidneys, we performed miRNA microarrays using RNA from kidneys of control and kidney-specific-cadherin (Ksp)/cre;Kif3a F/F (Kif3a-KO) mice, an animal model of PKD. The miR-17~92 cluster in cancer pathogenesis.

2009-12-15 The miR-17-92 cluster is often amplified or overexpressed in human cancers and has recently emerged as the prototypical oncogenic polycistron miRNA.
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Klusteret miR-17/92: en omfattande uppdatering av dess genomik, genetik, funktioner Genomisk representation av den humana miR-17-92-klustervärdgenen

Patel V (1), Williams D, Hajarnis S, Hunter R, Pontoglio M, Somlo S, Igarashi P. The paralogous miRNA gene clusters that give rise to miR-17 family microRNAs (miR-17~92, miR-106a~363, and miR-106b~25) have been implicated in a wide variety of malignancies and are sometimes referred to as oncomirs. The oncogenic potential of these non-protein encoding genes was first identified in mouse viral tumorigenesis screens. Unlike most protein coding genes, mir-17-92is a polycistronic miRNA cluster that contains multiple miRNA components, each of which has a potential to regulate hundreds of target mRNAs. This unique gene structure of mir-17-92may underlie the molecular basis for its pleiotropic functions in a cell type- and context-dependent manner.

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Absence of miR-17-92 leads to a reduction in oligodendrocyte number in vivo and we find that the expression of these miRNAs in primary cultures of

that the miR-17-92 cluster regulates adult neurogenesis in the subventricular zone (SVZ) (12). However, the in vivo effect of the miR-17-92 cluster on adult neurogenesis in the hippocampus and consequent neurobehavioral function, especially learning and memory, has not been investigated. In the present study, by specific ablation of this cluster in 2009-02-24 Microarray profiling of cultured oligodendrocytes identified the miR-17-92 miRNA cluster as highly enriched in oligodendrocytes. We specifically deleted the miR-17-92 cluster in oligodendrocytes using 2,3 -cyclic nucleotide 3 phosphodiesterase (Cnp)-Cre mice. Absence of miR-17-92 leads to a reduction in oligodendrocyte number in vivo and we Abstract: The human polycistronic miRNA cluster miR-17-92 is frequently overexpressed in hematopoietic malignancies and cancers. Its transcription is in part controlled by an E2F-regulated host gene promoter. An intronic A/T-rich region directly upstream of the miRNA coding region also contributes to cluster expression.