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      circ_0001730 promotes proliferation and invasion via the miR-326/Wnt7B axis in glioma cells

      1 , 2 , 3 , 4 , 2 , 5
      Epigenomics
      Future Medicine Ltd

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          Abstract

          Aim: To study the role of circRNA (circ_0001730) in glioblastoma. Materials & methods: The interaction between circ_0001730 and miR-326 was confirmed by FISH, RNA pull down, RNA-binding protein immunoprecipitation and luciferase reporter assays. Cell proliferation and growth were determined by MTT, EdU and colony formation assays. Cell migration was assessed by the Boyden assay. Results: The levels of circ_0001730 were elevated in glioblastoma cell lines and tissues. circ_0001730 downregulation suppressed migration and proliferation in glioblastoma cells. SP1 bounds to the promoter of circ_0001730 host gene EPHB4 thereby increasing the expression of circ_0001730. circ_0001730 activated the Wnt/β-catenin pathway via the miR-326/Wnt7B axis. Conclusion: circ_000173 promoted growth and invasion in glioblastoma cells via the miR-326/Wnt7B axis.

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          Most cited references36

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          Circular RNAs are a large class of animal RNAs with regulatory potency.

          Circular RNAs (circRNAs) in animals are an enigmatic class of RNA with unknown function. To explore circRNAs systematically, we sequenced and computationally analysed human, mouse and nematode RNA. We detected thousands of well-expressed, stable circRNAs, often showing tissue/developmental-stage-specific expression. Sequence analysis indicated important regulatory functions for circRNAs. We found that a human circRNA, antisense to the cerebellar degeneration-related protein 1 transcript (CDR1as), is densely bound by microRNA (miRNA) effector complexes and harbours 63 conserved binding sites for the ancient miRNA miR-7. Further analyses indicated that CDR1as functions to bind miR-7 in neuronal tissues. Human CDR1as expression in zebrafish impaired midbrain development, similar to knocking down miR-7, suggesting that CDR1as is a miRNA antagonist with a miRNA-binding capacity ten times higher than any other known transcript. Together, our data provide evidence that circRNAs form a large class of post-transcriptional regulators. Numerous circRNAs form by head-to-tail splicing of exons, suggesting previously unrecognized regulatory potential of coding sequences.
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            Natural RNA circles function as efficient microRNA sponges.

            MicroRNAs (miRNAs) are important post-transcriptional regulators of gene expression that act by direct base pairing to target sites within untranslated regions of messenger RNAs. Recently, miRNA activity has been shown to be affected by the presence of miRNA sponge transcripts, the so-called competing endogenous RNA in humans and target mimicry in plants. We previously identified a highly expressed circular RNA (circRNA) in human and mouse brain. Here we show that this circRNA acts as a miR-7 sponge; we term this circular transcript ciRS-7 (circular RNA sponge for miR-7). ciRS-7 contains more than 70 selectively conserved miRNA target sites, and it is highly and widely associated with Argonaute (AGO) proteins in a miR-7-dependent manner. Although the circRNA is completely resistant to miRNA-mediated target destabilization, it strongly suppresses miR-7 activity, resulting in increased levels of miR-7 targets. In the mouse brain, we observe overlapping co-expression of ciRS-7 and miR-7, particularly in neocortical and hippocampal neurons, suggesting a high degree of endogenous interaction. We further show that the testis-specific circRNA, sex-determining region Y (Sry), serves as a miR-138 sponge, suggesting that miRNA sponge effects achieved by circRNA formation are a general phenomenon. This study serves as the first, to our knowledge, functional analysis of a naturally expressed circRNA.
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              Circular RNAs in the Mammalian Brain Are Highly Abundant, Conserved, and Dynamically Expressed.

              Circular RNAs (circRNAs) are an endogenous class of animal RNAs. Despite their abundance, their function and expression in the nervous system are unknown. Therefore, we sequenced RNA from different brain regions, primary neurons, isolated synapses, as well as during neuronal differentiation. Using these and other available data, we discovered and analyzed thousands of neuronal human and mouse circRNAs. circRNAs were extraordinarily enriched in the mammalian brain, well conserved in sequence, often expressed as circRNAs in both human and mouse, and sometimes even detected in Drosophila brains. circRNAs were overall upregulated during neuronal differentiation, highly enriched in synapses, and often differentially expressed compared to their mRNA isoforms. circRNA expression correlated negatively with expression of the RNA-editing enzyme ADAR1. Knockdown of ADAR1 induced elevated circRNA expression. Together, we provide a circRNA brain expression atlas and evidence for important circRNA functions and values as biomarkers.
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                Author and article information

                Contributors
                Journal
                Epigenomics
                Epigenomics
                Future Medicine Ltd
                1750-1911
                1750-192X
                August 2019
                August 2019
                : 11
                : 11
                : 1335-1352
                Affiliations
                [1 ]Department of Oncology (Section 3), Gaozhou People’s Hospital, Gaozhou, Guangdong, PR China
                [2 ]Department of internal medicine, Affiliated Cancer Hospital & Institute of Guangzhou Medical University, Guangzhou, PR China
                [3 ]Department of Cancer Biology Program, Cancer Biology Program, Fox Chase Cancer Center, Philadelphia, PA 215, USA
                [4 ]Department of internal medicine, Yanling Hospital of Southern Medical University, Guangzhou, PR China
                [5 ]Department of Pharmacy, Maoming People’s Hospital, Maoming, Guangdong, PR China
                Article
                10.2217/epi-2019-0121
                31304776
                d5ecb9ea-19c6-41d0-8ab4-0fa04683e1f2
                © 2019
                History

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