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      OncoTargets and Therapy (submit here)

      This international, peer-reviewed Open Access journal by Dove Medical Press focuses on the pathological basis of cancers, potential targets for therapy and treatment protocols to improve the management of cancer patients. Publishing high-quality, original research on molecular aspects of cancer, including the molecular diagnosis, since 2008. Sign up for email alerts here. 50,877 Monthly downloads/views I 4.345 Impact Factor I 7.0 CiteScore I 0.81 Source Normalized Impact per Paper (SNIP) I 0.811 Scimago Journal & Country Rank (SJR)

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      Latest Advances of Long Non-Coding RNA SNHG5 in Human Cancers

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          Abstract

          Long non-coding RNAs (lncRNAs) have been potent regulators in the initiation and development of human cancers regarding their biological roles in the modulation of dosage compensation effect, epigenetics and cell differentiation. Recently, aberrant expression of lncRNA small nucleolar RNA host gene 5 (SNHG5) has been observed in various solid tumors, which was intently correlated with tumor range, metastasis, pathological stage and prognosis. Additional mechanical investigation disclosed that SNHG5 was involved in multiple cellular activities, including proliferation, migration, invasion, cell-cycle, apoptosis and autophagy, via targeting miRNAs, signaling pathways and other biological molecules or proteins. In this review, we summarized the latest advances made towards understanding the roles of SNHG5 in human cancers and further discussed potential methods that could be adopted for clinical interventions.

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          The lncRNA SNHG5/miR-32 axis regulates gastric cancer cell proliferation and migration by targeting KLF4

          Lianmei Zhao, Taotao Han, Yanshuang Li … (2017)
          Long noncoding RNAs (lncRNAs) are emerging as important regulators in cellular processes, including the development, proliferation, and migration of cancer cells. We have demonstrated in a prior study that small nucleolar RNA host gene 5 (SNHG5) is dysregulated in gastric cancer (GC). To further explore the underlying mechanisms of SNGH5 function in the development of GC, in this study, we screened the microRNAs interacting with SNHG5 and elucidated their roles in GC. We showed that SNHG5 contains a putative miR-32-binding site and that deletion of this site abolishes the responsiveness to miR-32. Suppression of SNHG5 expression by miR-32 was found to be Argonaute (Ago)2-dependent. Immunoprecipitation showed that SNHG5 could be pulled down from the Ago-2 complex with miR-32. Furthermore, it was reported that Kruppel-like factor 4 (KLF4) is a target gene of miR-32. In agreement with SNHG5 being a decoy for miR-32, we showed that KLF4 suppression by miR-32 could be partially rescued by SNHG5 overexpression, whereas miR-32 mimic rescued SNHG5 overexpression-mediated suppression of GC cell migration. In addition, we identified a negative correlation between the expression of SNHG5 and miR-32 in GC tissues. Furthermore, KLF4 expression was significantly downregulated in GC specimens, and a negative correlation between miR-32 and KLF4 expression and a positive correlation between KLF4 and SNHG5 expression levels were detected. Overall, this study demonstrated, for the first time, that the SNHG5/miR-32/KLF4 axis functions as an important player in GC cell migration and potentially contributes to the improvement of GC diagnosis and therapy.-Zhao, L., Han, T., Li, Y., Sun, J., Zhang, S., Liu, Y., Shan, B., Zheng D., Shi, J. The lncRNA SNHG5/miR-32 axis regulates gastric cancer cell proliferation and migration by targeting KLF4.
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            Long non-coding RNA SNHG5 promotes human hepatocellular carcinoma progression by regulating miR-26a-5p/GSK3β signal pathway

            Yarui Li, Dan Guo, Yan Zhao … (2018)
            Accumulating evidence have suggested that long non-coding RNAs (lncRNAs) had malfunctioning roles in the development of human cancers. The present study aimed to investigate the role of lncRNA small nucleolar RNA host gene 5 (SNHG5) in hepatocellular carcinoma (HCC) progression using human tissues and cell lines. The quantitative real-time PCR results showed that SNHG5 was up-regulated in both HCC tissues and hepatoma cell lines and was closely associated with tumor size, hepatitis B virus infection, histologic grade, TNM stage, and portal vein tumor thrombus (PVTT) in HCC patients. Knockdown of SNHG5 induced apoptosis and repressed cell cycle progression, cell growth, and metastasis in hepatoma cell lines, whereas overexpression of SNHG5 had the opposite effects. In vivo functional assay, xenograft tumors grown from SNHG5-knockdown cells had smaller mean volumes than the tumors grown from negative control cells. Further investigations showed that SNHG5 may act as a competing endogenous RNA by competitively binding miR-26a-5p and thereby modulating the derepression of downstream target GSK3β, which were further confirmed by luciferase reporter assay. Functionally, SNHG5 promotes tumor growth and metastasis by activating Wnt/β-catenin pathway and inducing epithelial to mesenchymal transition (EMT). Taken together, SNHG5 promotes HCC progression by competitively binding miR-26a-5p and regulating GSK3β and Wnt/β-catenin signal pathway.
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              Long non-coding RNA SNHG5 suppresses gastric cancer progression by trapping MTA2 in the cytosol.

              W L Zhao, H Guo, B. Zhou … (2016)
              Recently, intriguing new roles for some small nucleolar RNA host genes (SNHGs) in cancer have emerged. In the present study, a panel of SNHGs was profiled to detect aberrantly expressed SNHGs in gastric cancer (GC). The expression of SNHG5 was significantly downregulated in GC and was significantly associated with the formation of a tumor embolus and with the tumor, node and metastasis stage. SNHG5 was a long non-coding RNA, which was a class of non-coding RNA transcripts longer than 200 nucleotides. SNHG5 suppressed GC cell proliferation and metastasis in vitro and in vivo. Furthermore, SNHG5 exerted its function through interacting with MTA2, preventing the translocation of MTA2 from the cytoplasm into the nucleus. SNHG5 overexpression led to significant increases in the acetylation levels of histone H3 and p53, indicating that SNHG5 might affect acetylation by trapping MTA2 in the cytosol, thereby interfering with the formation of the nucleosome remodeling and histone deacetylation complex. This study is the first to demonstrate that SNHG5 is a critical and powerful regulator that is involved in GC progression through trapping MTA2 in the cytosol. These results imply that SNHG5 may be a novel therapeutic target for the treatment of GC.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Onco Targets Ther
                Journal ID (iso-abbrev): Onco Targets Ther
                Journal ID (publisher-id): OTT
                Journal ID (pmc): ott
                Title: OncoTargets and therapy
                Publisher: Dove
                ISSN (Electronic): 1178-6930
                Publication date (Electronic): 01 July 2020
                Publication date Collection: 2020
                Volume: 13
                Pages: 6393-6403
                Affiliations
                [1 ]Department of Neurosurgery, Third Affiliated Hospital of Soochow University , Changzhou, People’s Republic of China
                Author notes
                Correspondence: Wei Guan No. 185, Juqian Street, Changzhou, Jiangsu213003, People’s Republic of China Email guanwei1402@163.com
                Author information
                http://orcid.org/0000-0003-0033-1486
                Article
                Publisher ID: 252750
                DOI: 10.2147/OTT.S252750
                PMC ID: 7342554
                PubMed ID: 32753882
                SO-VID: 00afa168-6061-4adf-b192-51b000432c72
                Copyright © © 2020 Han et al.
                License:

                This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms ( https://www.dovepress.com/terms.php).

                History
                Date received : 06 March 2020
                Date accepted : 11 June 2020
                Page count
                Figures: 3, Tables: 2, References: 48, Pages: 11
                Funding
                This study was funded by the Changzhou Health and Family Planning Commission Youth Talent Science and Technology Project (WZ201811).
                Categories
                Subject: Review

                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: lncrna,snhg5,biomarker,therapeutic target,human cancers
                Data availability:
                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: lncrna, snhg5, biomarker, therapeutic target, human cancers

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