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慢病毒介导的抗微小RNA表达用于特异性抑制微小RNA功能。

Lentivirus-mediated antagomir expression for specific inhibition of miRNA function.

作者信息

Scherr Michaela, Venturini Letizia, Battmer Karin, Schaller-Schoenitz Michael, Schaefer Daniel, Dallmann Iris, Ganser Arnold, Eder Matthias

机构信息

Department of Hematology, Hemostasis, and Oncology, Hannover Medical School, Hannover, Germany.

出版信息

Nucleic Acids Res. 2007;35(22):e149. doi: 10.1093/nar/gkm971. Epub 2007 Nov 19.

Abstract

Micro RNAs (miRNA) regulate gene expression by hybridization and recruitment of multi-protein complexes to complementary mRNA target sequences. miRNA function can transiently be antagonized by antagomirs-chemically modified oligonucleotides complementary to individual miRNAs. Here, we describe the induction of stable loss-of-function phenotypes for specific miRNAs by lentivirus-mediated antagomir expression. Lentivirally expressed antagomirs are transcribed from a H1-promoter located within the lentiviral 3'LTR and were directed against miRNAs encoded on the polycistronic miR17-92 transcript. Functional silencing of miR-18a, miR-19b and miR-20a by the corresponding antagomirs specifically relieves miRNA-mediated reporter gene repression. Inhibition of miRNA function correlates to reduction of 'miRNA' amplification by miRNA-specific quantitative RT-PCR. Furthermore, protein expression of E2F-1, a known miR-20 target, is enhanced by lentivirally expressed anti-miR-20 antagomirs in a dose-dependent manner, whereas over-expression of miR-20a reduces E2F-1 levels. Finally, combined over-expression of specific miRNAs and antagomirs reveals individual and complementary functions of miR-18a and miR-20a and demonstrates specific miRNA impact on cell proliferation in a cell culture model.

摘要

微小RNA(miRNA)通过与多蛋白复合物杂交并将其募集到互补的mRNA靶序列来调节基因表达。抗miR寡核苷酸(与单个miRNA互补的化学修饰寡核苷酸)可短暂拮抗miRNA功能。在此,我们描述了通过慢病毒介导的抗miR表达诱导特定miRNA的稳定功能丧失表型。慢病毒表达的抗miR从位于慢病毒3'LTR内的H1启动子转录而来,靶向多顺反子miR17-92转录本上编码的miRNA。相应的抗miR对miR-18a、miR-19b和miR-20a的功能沉默特异性地减轻了miRNA介导的报告基因抑制。miRNA功能的抑制与通过miRNA特异性定量RT-PCR检测到的“miRNA”扩增减少相关。此外,慢病毒表达的抗miR-20抗miR以剂量依赖性方式增强了已知的miR-20靶标E2F-1的蛋白表达,而miR-20a的过表达降低了E2F-1水平。最后,特定miRNA和抗miR的联合过表达揭示了miR-18a和miR-20a的个体和互补功能,并在细胞培养模型中证明了特定miRNA对细胞增殖的影响。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/243a/2190705/d296cab67feb/gkm971f1a.jpg

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