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      SMARCC2 combined with c-Myc inhibits the migration and invasion of glioma cells via modulation of the Wnt/β-catenin signaling pathway

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          Abstract

          Glioma is the most common type of central nervous system tumor. SWItch/sucrose non-fermentable (SWI/SNF) is a tumor suppressor that serves an important role in epithelial-mesenchymal transition (EMT). The present study aimed to identify key molecules involved in the EMT process. SWI/SNF related, matrix associated, actin dependent regulator of chromatin subfamily c member 2 (SMARCC2) is mutated in and its expression is low in multiple types of cancer. SMARCC2 is the core subunit of the chromatin-remodeling complex, SWI/SNF. Relative mRNA SMARCC2 expression levels in human glioma tissue were analyzed via reverse transcription-quantitative PCR, whereas the protein expression levels were determined via immunohistochemistry staining. SMARCC2 expression was knocked down in glioma cells using small interfering RNA (si) and overexpressed by infection with adenovirus vectors carrying SMARCC2 cDNA. Wound healing and Transwell assays were performed to assess cell migration and invasion, respectively. Subsequently, immunofluorescence and western blotting were performed to analyze the expression levels of the oncogene c-Myc, which is associated with SMARCC2. SMARCC2 combines with C-MYC to downregulate its expression. Consistent with the results of the bioinformatics analysis, which revealed that the upregulated expression levels of SMARCC2 were associated with a more favorable prognosis in patients with glioma, the mRNA and protein expression levels of SMARCC2 were significantly upregulated in low-grade glioma tissues compared with high-grade glioma tissues. The results of the wound healing assay demonstrated that cell migration was significantly increased in the siSMARCC2-1/3 groups compared with the negative control (NC) group. By contrast, the migratory ability of cells was significantly reduced following transduction with adenovirus overexpressing SMARCC2, which upregulated the expression of SMARCC2, compared with the lentiviral vector-non-specific control (LVS-NC) group. The Transwell assay results further showed that SMARCC2 overexpression significantly inhibited the migratory and invasive abilities of U87MG and LN229 cells compared with the LVS-NC group. Co-immunoprecipitation assays were subsequently conducted to validate the binding of SMARCC2 and c-Myc; the results demonstrated that the expression of c-Myc was downregulated in adenovirus-transfected cells compared with LVS-NC-transfected cells. The results of the western blotting experiments demonstrated that the expression levels of N-cadherin, vimentin, snail family transcriptional repressor 1 and β-catenin were notably downregulated, whereas the expression levels of T-cadherin were markedly upregulated in cell lines stably overexpressing SMARCC2 compared with the LVS-NC group. In conclusion, the results of the present study suggested that SMARCC2 may inhibit Wnt/β-catenin signaling by regulating c-Myc expression in glioma. SMARCC2 regulates the EMT status of the glioblastoma cell line by mediating the expression of the oncogene C-MYC to inhibit its migration and invasion ability. Thus, SMARCC2 may function as a tumor suppressor or oncogene by regulating associated oncogenes or tumor suppressor genes.

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          Analysis of relative gene expression data using real-time quantitative PCR and the 2(-Delta Delta C(T)) Method.

          The two most commonly used methods to analyze data from real-time, quantitative PCR experiments are absolute quantification and relative quantification. Absolute quantification determines the input copy number, usually by relating the PCR signal to a standard curve. Relative quantification relates the PCR signal of the target transcript in a treatment group to that of another sample such as an untreated control. The 2(-Delta Delta C(T)) method is a convenient way to analyze the relative changes in gene expression from real-time quantitative PCR experiments. The purpose of this report is to present the derivation, assumptions, and applications of the 2(-Delta Delta C(T)) method. In addition, we present the derivation and applications of two variations of the 2(-Delta Delta C(T)) method that may be useful in the analysis of real-time, quantitative PCR data. Copyright 2001 Elsevier Science (USA).
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            Glioma

            Gliomas are primary brain tumours that are thought to derive from neuroglial stem or progenitor cells. On the basis of their histological appearance, they have been traditionally classified as astrocytic, oligodendroglial or ependymal tumours and assigned WHO grades I-IV, which indicate different degrees of malignancy. Tremendous progress in genomic, transcriptomic and epigenetic profiling has resulted in new concepts of classifying and treating gliomas. Diffusely infiltrating gliomas in adults are now separated into three overarching tumour groups with distinct natural histories, responses to treatment and outcomes: isocitrate dehydrogenase (IDH)-mutant, 1p/19q co-deleted tumours with mostly oligodendroglial morphology that are associated with the best prognosis; IDH-mutant, 1p/19q non-co-deleted tumours with mostly astrocytic histology that are associated with intermediate outcome; and IDH wild-type, mostly higher WHO grade (III or IV) tumours that are associated with poor prognosis. Gliomas in children are molecularly distinct from those in adults, the majority being WHO grade I pilocytic astrocytomas characterized by circumscribed growth, favourable prognosis and frequent BRAF gene fusions or mutations. Ependymal tumours can be molecularly subdivided into distinct epigenetic subgroups according to location and prognosis. Although surgery, radiotherapy and alkylating agent chemotherapy are still the mainstay of treatment, individually tailored strategies based on tumour-intrinsic dominant signalling pathways and antigenic tumour profiles may ultimately improve outcome. For an illustrated summary of this Primer, visit: http://go.nature.com/TXY7Ri.
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              Mechanisms of action and regulation of ATP-dependent chromatin-remodelling complexes

              Nucleosome-remodelling complexes can slide or eject histones, or incorporate histone variants, but they share an ATPase–translocase 'motor' and a common DNA translocation mechanism. In a unifying 'hourglass' model of remodeller function, the different remodeller subfamilies use different modules for targeting to nucleosomes but converge on a DNA translocation mechanism and then diverge again to achieve various outcomes.
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                Author and article information

                Journal
                Mol Med Rep
                Mol Med Rep
                Molecular Medicine Reports
                D.A. Spandidos
                1791-2997
                1791-3004
                August 2021
                02 June 2021
                02 June 2021
                : 24
                : 2
                : 551
                Affiliations
                [1 ]Department of Neurosurgery, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong 510515, P.R. China
                [2 ]Department of Hematology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong 510515, P.R. China
                [3 ]Nanfang Neurology Research Institution, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong 510515, P.R. China
                [4 ]Nanfang Glioma Centre, Guangzhou, Guangdong 510515, P.R. China
                Author notes
                Correspondence to: Dr Qiang Zhou or Professor Yuntao Lu, Department of Neurosurgery, Nanfang Hospital, Southern Medical University, 1838 Guangzhou Avenue North, Guangzhou, Guangdong 510515, P.R. China, E-mail: ellsonchou@ 123456163.com , E-mail: 947804460@ 123456qq.com
                Article
                MMR-0-0-12190
                10.3892/mmr.2021.12190
                8185515
                34080022
                02bcbe5b-7510-41c7-a50d-c92b2fee5ca2
                Copyright: © Li et al.

                This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

                History
                : 29 July 2020
                : 19 March 2021
                Funding
                Funded by: National Natural Science Foundation of China, open-funder-registry 10.13039/501100001809;
                Award ID: 81802830
                The present study was supported by the National Natural Science Foundation of China (grant no. 81802830).
                Categories
                Articles

                switch/sucrose non-fermentable,swi/snf related,matrix associated,actin dependent regulator of chromatin subfamily c member 2,c-myc,epithelial-mesenchymal transition,glioma

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