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Selective degradation of the miR-17 family members of the miR-17-92 cluster by human Cytomegalovirus

ABSTRACT: miRNA microarrays were used to investigate host miRNA expression profiles during HCMV clinical strain infection. Human foreskin fibroblasts (HFFs) were infected with the HCMV clinical strain Toledo. To mimic the attenuated strain, we used ToledoΔ15kb, which lacks the 15-kb genomic segment in the UL/b’ region.

ORGANISM(S): Homo sapiens

PROVIDER: GSE43761 | GEO | 2013/05/09

SECONDARY ACCESSION(S): PRJNA187360

REPOSITORIES: GEO

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Selective degradation of the miR-17 family members of the miR-17-92 cluster by human Cytomegalovirus

Project description:miRNA microarrays were used to investigate host miRNA expression profiles during HCMV clinical strain infection. Human foreskin fibroblasts (HFFs) were infected with the HCMV clinical strain Toledo. To mimic the attenuated strain, we used ToledoM-NM-^T15kb, which lacks the 15-kb genomic segment in the UL/bM-bM-^@M-^Y region. Changes in miRNA expression upon HCMV infection. Human foreskin fibroblasts (HFFs) were infected with Toledo-WT or ToledoM-NM-^T15kb for miRNA microarray (5 MOI). The miRNA expression levels of virus-infected HFFs at 24 or 72 hpi have been compared with those for the noninfected control.

2013-05-09 | E-GEOD-43761 | biostudies-arrayexpress

miR-17-92 sustains lymphoma growth by fine-tuning MYC

Project description:The synergism between c-MYC and miR-17-19b, a truncated version of the miR-17-92 cluster, is well documented during tumor initiation. However, little is known about miR-17-19b function in established cancers. Here we investigate the role of miR-17-19b in c-MYC-driven lymphomas by integrating SILAC-based quantitative proteomics, transcriptomics and 3’ UTR analysis upon miR-17-19b overexpression. We identify over one hundred novel miR-17-19b targets, of which 40% are co-regulated by c-MYC. Down-regulation of a new miR-17/20 target Chek2 increases the recruitment of HuR to c-MYC transcripts, resulting in the inhibition of c-MYC translation and thus interfering with in vivo tumor growth. Hence, in established lymphomas, miR-17-19b fine-tunes c-MYC activity through a tight control of its function and expression, ultimately ensuring cancer cell homeostasis. Our data highlight the plasticity of miRNA function, reflecting changes in the mRNA landscape and 3’ UTR shortening at different stages of tumorigenesis.

2015-11-06 | PXD002810 | Pride

Differential regulation of aggressive features in melanoma cells by members of the miR-17-92 complex

Project description:The various roles of microRNAs (miRNAs) in controlling the phenotype of cancer cells are the focus of contemporary research efforts. We have recently shown that miR-17 directly targets the ADAR1 gene and thereby enhances melanoma cell aggressiveness. miR-17 and miR-20a belong to the miR-17/92 complex, and their mature forms are identical except for two non-seed nucleotides. Nevertheless, here we show that these two miRNAs carry markedly different effects on melanoma cells. A strong positive correlation was observed between the expression of miR-17 and miR-20a among various melanoma cultures. Luciferase assays showed that miR-17 but not miR-20a directly targets the 3' untranslated region of the ADAR1 gene. Ectopic expression of these miRNAs in melanoma cells differentially alters the expression of five exemplar TargetScan-predicted target genes ADAR1, ITGB8, TGFBR2, MMP2 and VEGF-A. Whole genome expression microarrays confirm a markedly differential effect on the transcriptome. Functionally, over-expression of miR-20a but not of miR-17 in melanoma cells inhibits net proliferation in-vitro. The differential functional effect was observed following ectopic expression of the mature miRNA or of the pre-miRNA sequences. This suggests that the two non-seed nucleotides dictate target sequence recognition and overall functional relevance. These miRNAs are clearly not redundant in melanoma cell biology.

2014-12-31 | GSE57158 | GEO

MiR-17-92 and miR-221/222 cluster members target KIT and ETV1 in human gastrointestinal stromal tumours.

Project description: Not available

| S-EPMC3776993 | biostudies-literature

MiR-17-92 cluster promotes hepatocarcinogenesis.

Project description: Not available

| S-EPMC4794620 | biostudies-literature

miR-17-92 explains MYC oncogene addiction.

Project description: Not available

| S-EPMC4905255 | biostudies-other

Differential regulation of aggressive features in melanoma cells by members of the miR-17-92 complex.

Project description: Not available

| S-EPMC4077061 | biostudies-literature

A biogenesis step upstream of Microprocessor controls miR-17~92 expression

Project description:The precise control of miR-17~92 microRNA (miRNA) is essential for normal development and overexpression of certain miRNAs from this cluster is oncogenic. Here we find the relative expression of the six miRNAs processed from the primary (pri-miR-17~92) transcript is dynamically regulated during embryonic stem cell differentiation. We identify a new miRNA biogenesis intermediate, termed ‘progenitor-miRNA’ (pro-miRNA), that is an efficient substrate for Microprocessor. An autoinhibitory 5’ RNA fragment is cleaved to generate pro-miRNA and selectively license Microprocessor-mediated production of pre-miR-17, -18a, -19a, 20a, and -19b. Using genetic, biochemical, and structural methods we define two complementary cis-regulatory repression domains required for the formation of this inhibitory RNA conformation. We find the endonuclease CPSF3 (CPSF73), and the Spliceosome-associated ISY1 are required for pro-miRNA biogenesis and expression of all miRNAs within the cluster except miR-92. Thus, developmentally regulated generation of pro-miRNA explains the posttranscriptional control of miR-17~92 expression in development.

2015-05-11 | GSE68699 | GEO

Oncogenic biogenesis of pri-miR-17~92

Project description:The microRNAs encoded by the miR-17~92 polycistron are commonly overexpressed in cancer and orchestrate a wide range of oncogenic functions. Here, we identify a novel mechanism for miR-17~92 oncogenic function through the disruption of endogenous miRNA processing. We show that upon oncogenic overexpression of the miR-17~92 primary transcript (pri-miR-17~92), the Microprocessor complex remains associated with partially processed intermediates that aberrantly accumulate. These intermediates reflect a series of hierarchical and conserved steps in the early processing of the pri-miR-17~92 transcript. Encumbrance of the Microprocessor by miR-17~92 intermediates leads to the broad, but selective, downregulation of co-expressed polycistronic miRNAs, including miRNAs derived from tumour suppressive miR-34b/c, and from the Dlk1-Dio3 polycistrons. We propose that the newly identified steps of polycistronic miR-17~92 biogenesis contribute to the oncogenic re-wiring of gene regulation networks. Our results reveal new functional paradigms for polycistronic miRNAs in cancer.

2019-05-20 | GSE130282 | GEO

Protein profiling upon miR-17-92 induction.

Project description:Methionine COFRADIC combined with Arg and Lys SILAC labeling was used to quantify proteins upon induction of miR-17-92 in SHEP neuroblastoma cells. Differently labeled cells treated with tetracycline for 72 h or left untreated, were harvested and mixed lysates were analyzed by methionine COFRADIC to isolate methionyl peptides followed by identification of these peptides by LC-MS/MS and subsequent quantification.

2010-12-10 | PRD000321 | Pride

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