including an oncogenic miR-17-92 cluster and oncosuppressive miR-143-145 cluster, and snoRNAs in synchronous CRC. Differential miRNA rather than

The Oncogenic Relevance of miR-17-92 Cluster and Its Paralogous miR-106b- 25 and miR-106a-363 Clusters in Brain Tumors. by. Renata Gruszka. * and.

A common secondary genomic alteration detected in MCL is chromosome 13q31-q32 gain/amplification, which targets a microRNA (miRNA) cluster, miR-17∼92. miR-17~92 miRNA cluster promotes kidney cyst growth in polycystic kidney disease. 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.

The miR-17/92 cluster has been implicated in tant miRNA of the miR-17-92 cluster in c-Myc-induced lymphomagenesis, both groups studied the mRNA tar-gets of miR-19. Mu et al. (2009) analyzed changes in gene expression in a lymphoma cell line derived from a mouse homozygous for the inducible deletion of the miR-17-92 cluster and heterozygous for Em-Myc. They found 568 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. A polycistronic miRNA cluster miR-17-92 plays a role in the control of cell proliferation and angiogenesis. This cluster consists of seven miRNAs: miR-17-5p, miR-17-3p, miR-18a, miR-19a, miR-19b, miR-20a, and miR-92.

av K Edvardsson · 2011 — miRNA pool in colon cancer cells.

Members of the miRNA gene cluster can coordinate the regulation of certain processes or play a similar role in the same biological process, ensuring biological activity occurs in a normal and orderly fashion. miR-17-92 encodes a miRNA precursor and produces 7 mature miRNA molecules that belong to 4 miRNA …

Proper miR-17~92 cluster is necessary for normal lung development and alterations in expression are reported in other pulmonary diseases. The overall hypothesis for our work is that altered miRNA expression profiles were significantly different between malignant and benign tissue and between cancer subgroups according to ER− status, grade and molecular subtype. miRNAs in the miR-17-92 cluster and miR-17 family were overexpressed in high grade and triple-negative tumors associated with aggressive behavior. 2013-11-11 The median survival of patients with mantle cell lymphoma (MCL) ranges from 3 to 5 years with current chemotherapeutic regimens.

MEK Inhibitor Suppresses Expression of the miR-17-92 Cluster with G1-Phase Arrest in HT-29 Human Colon Cancer Cells and MIA PaCa-2 Pancreatic Cancer

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.

miR-17-92 encodes a miRNA precursor and produces 7 mature miRNA molecules that belong to 4 miRNA families. To investigate whether this miRNA panel might be used as a non-invasive biomarker, miR-17/92 cluster expression profile was analyzed in peripheral blood. Cell-free plasma and plasma exosomes of RC patients were examined at the diagnosis and, to be able to associate miRNA profiles with treatment outcomes, 6 and 12 months later, spanning thus the period of chemotherapy and recovery. Now more than 300 miRNA clusters are found in the human genome, including miR-183-96-182 cluster, miR-35-41 cluster, miR-17-92 cluster and so on. MiR-17-92 cluster is involved in the development of multiple organs in mammals and closely related to the development and occurrence of tumors, thus it receives widespread attention in the world [ 9 ].
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Herein, we used sequence-based design of structure-specific ligands to target a common structure in the Dicer Members of the miRNA gene cluster can coordinate the regulation of certain processes or play a similar role in the same biological process, ensuring biological activity occurs in a normal and orderly fashion.

9628 - 9632 View Record in Scopus Google Scholar The miR-17-92 cluster is a typical highly conserved polycistronic miRNA cluster, which is located in the human chromosome 13 open reading frame 25 (C13orf25), encoding six mature miRNAs, including miR-17, miR-18a, miR-19a, miR-19b, miR-20a and miR-92a (10). Proper miR-17~92 cluster is necessary for normal lung development and alterations in expression are reported in other pulmonary diseases. The overall hypothesis for our work is that altered miRNA expression profiles were significantly different between malignant and benign tissue and between cancer subgroups according to ER− status, grade and molecular subtype. miRNAs in the miR-17-92 cluster and miR-17 family were overexpressed in high grade and triple-negative tumors associated with aggressive behavior.
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2018-10-01

2013; 288:12478–12488. doi: 10.1074/jbc.M112.449025.

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Adipogenesis involves cell proliferation and differentiation, both of which have been shown to be regulated by micro (mi)RNA. During mouse preadipocyte 3T3L1 cell differentiation, we found that miR-17-92, a miRNA cluster that promotes cell proliferation in various cancers, was significantly up-regulated at the clonal expansion stage of adipocyte differentiation.

The miR-17-92 gene cluster, a polycistron encoding six microRNAs (miRNA), is frequ … In mammalian cells, activation of oncogenes usually triggers innate tumor-suppressing defense mechanisms, including apoptosis and senescence, which are compromised by additional mutations before cancers are developed. 3. Expression and regulation of the miRNA-17-92 cluster in tumor cells Expression and functions of miR-17/20a. The miRNA-17-92 cluster may be highly expressed in a wide range of tumor cells and types of cancer, such as lung, breast, pancreatic, prostate and thyroid cancer, as well as lymphomas (7,14). Therefore, it is also referred to as MiR-17-92 cluster is an oncogenic miRNA cluster that is implicated in several cancers, although its role in hepatocarcinogenesis has not been clearly defined. In this study, we show that the miR-17-92 cluster is highly expressed in human hepatocellular carcinoma (HCC) tissues compared to the non-tumorous liver tissues by RT-PCR and in situ hybridization analyses. In humans, the activating mutations of miR-17~92 have been identified in non-Hodgkin's lymphoma, whereas the miRNA constituents of the clusters are overexpressed in a multiple cancer types.