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Small RNA and High Molecular Weight RNA Deep Sequencing Analysis of miR-17~92 Mimics Transfected HeLa cells

ABSTRACT: Transient transfection of miRNA mimics are widely used to alter microRNA expression in cells. The goal of this study is to perform small RNA deep sequencing analysis of HeLa cells transfected with miR-17~92 cluster and address potential source of non-specific effects caused by this approach.

ORGANISM(S): Homo sapiens

PROVIDER: GSE73099 | GEO | 2015/09/17

SECONDARY ACCESSION(S): PRJNA296037

REPOSITORIES: GEO

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Small RNA and High Molecular Weight RNA Deep Sequencing Analysis of miR-17~92 Mimics Transfected HeLa cells

Project description:Transient transfection of miRNA mimics are widely used to alter microRNA expression in cells. The goal of this study is to perform small RNA deep sequencing analysis of HeLa cells transfected with miR-17~92 cluster and address potential source of non-specific effects caused by this approach. HeLa cells were cultured as adherent cells. Equal molar concentration of miRNA mimics of miR-17~92 (100nM, 16.7nM each) were transfected and harvedsted at 6h post-transfection for small RNA deep sequencing analysis.

2015-09-17 | E-GEOD-73099 | biostudies-arrayexpress

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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.

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Mouse gene expression profile after transfected with miR-27a mimics and mimic NC in Raw

Project description:Microarry analysis of mouse gene expression profile after transfected with miR-27a mimics (27a-7) and mimic NC (NC-9) Goal was to determine the effects of miR-27a transfection on global gene expression.

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Project description:We have generated a miR-17~92 transgene and fl/fl allele whose expression can be turned on and off conditionally by Cre recombinase. The mice were crossed to CD19-Cre mice to turn on and off the expression of miR-17~92 specifically in B cells and stimulated LPS/IL-4 for 25.5hr. tKO mice were generated in the miR-106a-363-/-;miR-106b-25-/- background, so that all three homologous cluster of miR-17~92 family miRNAs are deleted in B cells.

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The role of microRNA miR-17-92 in MYC oncogene addiction

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