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      Long noncoding RNA SNHG17 induced by YY1 facilitates the glioma progression through targeting miR-506-3p/CTNNB1 axis to activate Wnt/β-catenin signaling pathway

      research-article
      1 , 1 , 2 , 3 ,
      Cancer Cell International
      BioMed Central
      SNHG17, YY1, miR-506-3p, CTNNB1, Glioma

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          Abstract

          Background

          Glioma is one of the most widely diagnosed malignancies worldwide. It has been reported that long noncoding RNAs (lncRNAs) are participators in the tumorgenesis of cancers. Nevertheless, the role and function of lncRNA SNHG17 among glioma is unclear.

          Methods

          RT-qPCR revealed SNHG17, YY1, miR-506-3p, CTNNB1 expression among glioma cells. CCK-8, colony formation, EdU, flow cytometry, TUNEL and western blot assays revealed the function of SNHG17 in glioma. RIP uncovered SNHG17, miR-506-3p and CTNNB1 enrichment in RISC complex. Luciferase reporter assays and RNA pull down revealed interaction of miR-506-3p with SNHG17 and CTNNB1.

          Results

          SNHG17 expression was up-regulated in glioma tissues and cells. SNHG17 silence attenuated cell proliferation and promoted apoptosis and repressed tumor growth. Moreover, SNHG17 was up-regulated by transcription factor YY1. Mechanistically, SNHG17 activated Wnt/β-catenin signaling pathway in glioma. CTNNB1 was referred to as the mRNA of β-catenin, we validated that SNHG17 bound to miR-506-3p to induce CTNNB1 and activate Wnt/β-catenin signaling pathway. Rescue experiments indicated that CTNNB1 overexpression abolished the inhibitory effects of SNHG7 inhibition on glioma progression.

          Conclusions

          The findings that YY1-induced SNHG17 facilitated the glioma progression through targeting miR-506-3p/CTNNB1 axis to activate Wnt/β-catenin signaling pathway offered a brand-new prospects to molecular-targeted treatment for glioma.

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          Most cited references20

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          LincRNA landscape in human lymphocytes highlights regulation of T cell differentiation by linc-MAF-4

          Long non-coding-RNAs are emerging as important regulators of cellular functions but little is known on their role in human immune system. Here we investigated long intergenic non-coding-RNAs (lincRNAs) in thirteen T and B lymphocyte subsets by RNA-seq analysis and de novo transcriptome reconstruction. Over five hundred new lincRNAs were identified and lincRNAs signatures were described. Expression of linc-MAF-4, a chromatin-associated TH1-specific lincRNA, was inversely correlated with MAF, a TH2-associated transcription factor. Linc-MAF-4 down-regulation skewed T cell differentiation toward TH2. We identified a long-distance interaction between linc-MAF-4 and MAF genomic regions, where linc-MAF-4 associates with LSD1 and EZH2, suggesting linc-MAF-4 regulated MAF transcription by recruitment of chromatin modifiers. Our results demonstrate a key role of lincRNAs in T lymphocyte differentiation.
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            Knockdown of long non-coding RNA NEAT1 inhibits glioma cell migration and invasion via modulation of SOX2 targeted by miR-132

            Background A better understanding of the molecular mechanism involving lncRNA-miRNA-mRNA network underlying glioma genesis is beneficial to the treatment of glioma. This study was designed to investigate the role of lncRNA NEAT1, miR-132 and SOX2 interaction in glioma. Methods Microarray analysis was conducted to identify the differentially expressed lncRNAs in glioma tissues. The expression levels of NEAT1, miR-132 and SOX2 were determined by qRT-PCR and western blot. Proliferation of glioma cells was detected by MTT assay, while migration and invasion were determined by transwell assay. The target relationships were predicted by miRcode algorithm, and confirmed by dual luciferase reporter gene assay. Results NEAT1 was up-regulated in glioma. Knockdown of NEAT1 inhibited glioma cells’ viability, migration and invasion. MiR-132 was down-regulated while SOX2 was up-regulated in glioma cells. NEAT1 negatively regulated the expression of miR-132 in glioma while miR-132 targeted SOX2 to down-regulate its expression. Conclusion NEAT1 promoted glioma development by promoting SOX2 expression through suppressing miR-132. Electronic supplementary material The online version of this article (10.1186/s12943-018-0849-2) contains supplementary material, which is available to authorized users.
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              LncRNA SPRY4-IT1 sponges miR-101-3p to promote proliferation and metastasis of bladder cancer cells through up-regulating EZH2.

              Emerging evidences have indicated that long non-coding RNAs (LncRNAs) play vital roles in cancer development and progression. Previous studies have suggested that overexpression of SPRY4-IT1 predicates poor prognosis and promotes tumor progress in several cancers. However, the underlying mechanism of SPRY4-IT1 in bladder cancer remains unknown. In this study, we found that SPRY4-IT1 knockdown induced inhibition of cell proliferation, cell migration and invasion ability, and caused promotion of apoptosis in bladder cancer both in vitro and in vivo. Mechanistically, knockdown of SPRY4-IT1 increased the expression of miR-101-3p and subsequently inhibited the expression of EZH2 at posttranscriptional level. Importantly, SPRY4-IT1 could directly interact with miR-101-3p and down-regulation of miR-101-3p efficiently reversed the suppression of EZH2 induced by SPRY4-IT1 shRNA. Thus, SPRY4-IT1 positively regulated the expression of EZH2 through sponging miR-101-3p, and played an oncogenic role in bladder cancer progression. Together, our study elucidates the role of LncRNA SPRY4-IT1 as a miRNA sponge in bladder cancer, and sheds new light on LncRNA-directed diagnostics and therapeutics in bladder cancer.
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                Author and article information

                Contributors
                pengde494206498@163.com
                Journal
                Cancer Cell Int
                Cancer Cell Int
                Cancer Cell International
                BioMed Central (London )
                1475-2867
                28 January 2020
                28 January 2020
                2020
                : 20
                : 29
                Affiliations
                [1 ]GRID grid.412633.1, Reception Office, , The First Affiliated Hospital of Zhengzhou University, ; Zhengzhou, 450000 Henan China
                [2 ]Department of Pathogen Biology and Immunology, Henan Medical College, Zhengzhou, 450000 Henan China
                [3 ]GRID grid.412633.1, The First Affiliated Hospital of Zhengzhou University, ; No. 186 Worker Road, Zhongyuan District, Zhengzhou, Henan China
                Author information
                http://orcid.org/0000-0003-3143-2204
                Article
                1088
                10.1186/s12935-019-1088-3
                6988207
                32669970
                c4bc2c6b-4cc2-43a9-ae28-8f5189b37792
                © The Author(s) 2020

                Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

                History
                : 22 August 2019
                : 23 December 2019
                Categories
                Primary Research
                Custom metadata
                © The Author(s) 2020

                Oncology & Radiotherapy
                snhg17,yy1,mir-506-3p,ctnnb1,glioma
                Oncology & Radiotherapy
                snhg17, yy1, mir-506-3p, ctnnb1, glioma

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