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      LncRNA SNHG3 promotes cell growth by sponging miR-196a-5p and indicates the poor survival in osteosarcoma

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          Abstract

          Abnormal expression of long noncoding RNAs (lncRNAs) is closely associated with the pathogenesis of multiple malignancies, and lncRNA small nucleolar RNA host genes (SNHGs) play critical roles in tumor progression. However, the mechanism by which SNHG3 contributes to osteosarcoma (OS) remains elusive. The association between SNHG3 expression and the clinicopathological characteristics in OS patients was analyzed using the TCGA (The Cancer Genome Atlas) dataset. Cell viability and colony number were estimated by MTT and colony formation assays. MiR-196a-5p-specific binding with SNHG3 or HOXC8 was confirmed by the luciferase report assay. As a result, the expression of SNHG3 was dramatically increased in OS tissue as compared with the adjacent normal tissues. High expression of SNHG3 was associated with tumor size and acted as an independent prognostic factor of poor survival in OS patients. Knockdown of SNHG3 inhibited cell viability and colony formation, but its overexpression reversed these effects. SNHG3 was further identified to act as a sponge of miR-196a-5p, which counteracted the tumor-promoting effects caused by SNHG3 in OS cells. The expression of miR-196a-5p had a negative correlation with SNHG3 and the poor survival in OS patients. In conclusion, lncRNA SNHG3 promoted cell growth by sponging miR-196a-5p and indicated a poor prognosis in OS patients.

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          Long noncoding RNA DANCR, working as a competitive endogenous RNA, promotes ROCK1-mediated proliferation and metastasis via decoying of miR-335-5p and miR-1972 in osteosarcoma

          Background Accumulating evidences indicate that non-coding RNAs (ncRNAs) including long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) acting as crucial regulators in osteosarcoma (OS). Previously, we reported that Rho associated coiled-coil containing protein kinase 1 (ROCK1), a metastatic-related gene was negatively regulated by microRNA-335-5p (miR-335-5p) and work as an oncogene in osteosarcoma. Whether any long non-coding RNAs participate in the upstream of miR-335-5p/ROCK1 axial remains unclear. Methods Expression of differentiation antagonizing non-protein coding RNA (DANCR) and miR-335-5p/miR-1972 in osteosarcoma tissues were determined by a qRT-PCR assay and an ISH assay. Osteosarcoma cells’ proliferation and migration/invasion ability changes were measured by a CCK-8/EDU assay and a transwell assay respectively. ROCK1 expression changes were checked by a qRT-PCR assay and a western blot assay. Targeted binding effects between miR-335-5p/miR-1972 and ROCK1 or DANCR were verified by a dual luciferase reporter assay and a RIP assay. In vivo experiments including a nude formation assay as well as a CT scan were applied to detect tumor growth and metastasis changes in animal level. Results In the present study, an elevated DNACR was found in osteosarcoma tissue specimens and in osteosarcoma cell lines, and the elevated DNACR was closely correlated with poor prognosis in clinical patients. Functional experiments illustrated that a depression of DANCR suppressed ROCK1-mediated proliferation and metastasis in osteosarcoma cells. The results of western blot assays and qRT-PCR assays revealed that DANCR regulated ROCK1 via crosstalk with miR-335-5p and miR-1972. Further cellular behavioral experiments demonstrated that DNACR promoted ROCK1-meidated proliferation and metastasis through decoying both miR-335-5p and miR-1972. Finally, the outcomes of in vivo animal models showed that DANCR promoted tumor growth and lung metastasis of osteosarcoma. Conclusions LncRNA DANCR work as an oncogene and promoted ROCK1-mediated proliferation and metastasis through acting as a competing endogenous RNA (ceRNA) in osteosarcoma. Electronic supplementary material The online version of this article (10.1186/s12943-018-0837-6) contains supplementary material, which is available to authorized users.
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            LncRNA SNHG12 promotes tumorigenesis and metastasis in osteosarcoma by upregulating Notch2 by sponging miR-195-5p

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              MicroRNA-196a promotes cervical cancer proliferation through the regulation of FOXO1 and p27Kip1

              Background: The phosphoinositide 3-kinase (PI3K)/Akt signalling pathway appears to be a key regulator in cervical carcinogenesis. However, the downstream regulatory mechanism of PI3K/Akt signalling remains largely unknown. Methods: The expression of miR-196a in cervical cancer cell lines and cervical cancer tissues was examined using real-time PCR. The effects of miR-196a on PI3K/Akt signalling and cellular proliferation were evaluated by bromodeoxyuridine labelling, 3-(4,5-Dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazoliumbromide, colony formation assays and luciferase assays. Results: The expression level of miR-196a was markedly increased in cervical cancer tissues and cell lines compared with normal cervical tissue and normal cervical squamous cells. Upregulation of miR-196a was correlated with advanced tumour stage and poor overall and recurrence-free survival in cervical cancer patients. Upregulation of miR-196a enhanced G1/S-phase transition and the proliferative ability of cervical cancer cells, whereas suppression of miR-196a had the opposite effect. Using bioinformatics and biological approaches, we showed that FOXO1 and p27Kip1, two key effectors of PI3K/Akt signalling, were direct targets of miR-196a. Conclusions: Our findings suggest that miR-196a has an important role in promoting human cervical cancer cell proliferation and may represent a novel therapeutic target of microRNA-mediated suppression of cell proliferation in cervical cancer.
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                Author and article information

                Journal
                Int J Immunopathol Pharmacol
                Int J Immunopathol Pharmacol
                IJI
                spiji
                International Journal of Immunopathology and Pharmacology
                SAGE Publications (Sage UK: London, England )
                0394-6320
                2058-7384
                09 January 2019
                2019
                : 33
                : 2058738418820743
                Affiliations
                [1 ]Department of Orthopedic Surgery, Jing’an District Zhabei Central Hospital, Shanghai, China
                [2 ]Department of Orthopedic Surgery, Shibei Hospital of Jingan District, Shanghai, China
                Author notes
                [*]Yong Zhang, Department of Orthopedic Surgery, Shibei Hospital of Jingan District, 4500 Gonghexin Road, Jingan District, Shanghai 200070, China. Email: 15921363659@ 123456163.com
                Article
                10.1177_2058738418820743
                10.1177/2058738418820743
                6329016
                3242f28d-8fa4-4421-86af-a314403e5d2c
                © The Author(s) 2019

                This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License ( http://www.creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages ( https://us.sagepub.com/en-us/nam/open-access-at-sage).

                History
                : 26 August 2018
                : 19 November 2018
                Categories
                Letter to the Editor
                Custom metadata
                January-December 2019

                growth,hoxc8,mir-196a-5p,osteosarcoma,snhg3
                growth, hoxc8, mir-196a-5p, osteosarcoma, snhg3

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