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      Correction to: EIF4A3-induced circular RNA MMP9 (circMMP9) acts as a sponge of miR-124 and promotes glioblastoma multiforme cell tumorigenesis

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          Abstract

          Correction to: Mol Cancer 17, 166 (2018) https://doi.org/10.1186/s12943-018-0911-0 Following the publication of the original article [1], authors found out that it contains a duplication error within Figs. 4h and 5b. The correct version of Figs. 4 and 5 are shown below. In addition, the correct version of Fig. 1 and Additional file 1 are also provided in this paper. Fig. 1. Characterization of circMMP9 in human GBM. a Clustered heat map showing tissue-specific circRNAs (top 20 upregulated and downregulated circRNAs), which are displayed on a scale from green (low) to red (high), between three human GBM tissues and adjacent normal tissues. The arrow represents the circRNA (hsa_circ_001162) with the greatest differential expression. b Detailed information for the top 20 upregulated and downregulated circRNAs according to the extent. c Schematic representation of circMMP9 formation. The splice junction sequence was Sanger sequenced, and the RNAs were detected via PCR. Divergent primers could produce circRNAs in cDNA but not in genomic DNA (gDNA); convergent primers could produce cDNA and gDNA. d The expression level of circMMP9 was detected by qRT-PCR in GBM tissues and adjacent normal brain tissues (n = 18, P < 0.05); GAPDH served as the internal control. e-f circMMP9 expression was measured using in situ hybridization (FISH) in GBM tissues and adjacent normal brain tissues (n = 18, P < 0.05). g-h Confocal FISH was performed to determine the location of circMMP9 in U87 and U251 cells Fig. 4 circMMP9 accelerates GBM cell proliferation, migration and invasion by targeting miR-124. a-d U87 cells were transfected with mock, circMMP9 plasmid, or circMMP9 plasmid and miR-124; U251 cells were transfected with mock, circMMP9 siRNA1 + 2, or circMMP9 siRNA1 + 2 and anti-miR-124. CCK-8 and colony formation assays were performed to assess the proliferation ability of the transfected U87 and U251 cells (***P < 0.001). Western blot assays were used to analyze the protein expression levels of PCNA and Ki67 in transfected U87 and U251 cells. e-h Transwell assays were performed to evaluate cell migration and invasion abilities (***P < 0.001). Western blot assays were used to analyze the protein expression levels of E-cadherin (E-cad), snail and vimentin in transfected U87 and U251 cells Fig. 5 circMMP9 upregulates CDK4 and AURKA via miR-124. a Flow chart to screen the targets of miR-124 in GBM. b CDK4 and AURKA expression was detected via IHC in GBM tissues and adjacent normal tissues. c The cells positive for CDK4 and AURKA were counted (***P < 0.001). d The protein expression levels of CDK4 and AURKA were measured by western blot assays in GBM tissues and adjacent normal tissues. e CDK4 and AURKA expression was evaluated by qRT-PCR in GBM tissues with high circMMP9 expression or low circMMP9 expression (P < 0.05). f U87 cells were transfected with mock, circMMP9 plasmid, or circMMP9 plasmid and miR-124. CDK4 and AURKA expression was detected by qRT-PCR and western blot assays (***P < 0.001). g U251 cells were transfected with mock, circMMP9 siRNA1 + 2, circMMP9 siRNA1 + 2 or anti-miR-124. CDK4 and AURKA expression was detected by qRT-PCR and western blot assays (***P < 0.001) Supplementary information Additional file 1 : Table S1. The primers used in this study

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          EIF4A3-induced circular RNA MMP9 (circMMP9) acts as a sponge of miR-124 and promotes glioblastoma multiforme cell tumorigenesis

          Background Circular RNAs (circRNAs) have been found to play critical roles in the development and progression of various cancers. However, little is known about the effects of the circular RNA network on glioblastoma multiforme (GBM). Methods A microarray was used to screen circRNA expression in GBM. Quantitative real-time PCR was used to detect the expression of circMMP9. GBM cells were transfected with a circMMP9 overexpression vector or siRNA, and cell proliferation, migration and invasion, as well as tumorigenesis in nude mice, were assessed to examine the effect of circMMP9 in GBM. Biotin-coupled miRNA capture, fluorescence in situ hybridization and luciferase reporter assays were conducted to confirm the relationship between circMMP9 and miR-124. Results In this study, we screened differentially expressed circRNAs and identified circMMP9 in GBM. We found that circMMP9 acted as an oncogene, was upregulated in GBM and promoted the proliferation, migration and invasion abilities of GBM cells. Next, we verified that circMMP9 served as a sponge that directly targeted miR-124; circMMP9 accelerated GBM cell proliferation, migration and invasion by targeting miR-124. Furthermore, we found that cyclin-dependent kinase 4 (CDK4) and aurora kinase A (AURKA) were involved in circMMP9/miR-124 axis-induced GBM tumorigenesis. Finally, we found that eukaryotic initiation factor 4A3 (eIF4A3), which binds to the MMP9 mRNA transcript, induced circMMP9 cyclization and increased circMMP9 expression in GBM. Conclusions Our findings indicate that eIF4A3-induced circMMP9 is an important underlying mechanism in GBM cell proliferation, invasion and metastasis through modulation of the miR-124 signaling pathway, which could provide pivotal potential therapeutic targets for the treatment of GBM. Graphical abstract Electronic supplementary material The online version of this article (10.1186/s12943-018-0911-0) contains supplementary material, which is available to authorized users.
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            Author and article information

            Contributors
            lianghaiqian711@163.com
            Journal
            Mol Cancer
            Mol Cancer
            Molecular Cancer
            BioMed Central (London )
            1476-4598
            30 October 2020
            30 October 2020
            2020
            : 19
            : 153
            Affiliations
            [1 ]Institute of Traumatic Brain Injury and Neurology, Characteristic Medical Center of Chinese People’s Armed Police Force, Tianjin, 300162 China
            [2 ]Department of Neurosurgery, Characteristic Medical Center of Chinese People’s Armed Police Force, Tianjin, 300162 China
            [3 ]GRID grid.265021.2, ISNI 0000 0000 9792 1228, Department of Basic Medicine, , Tianjin Medical College, ; Tianjin, 300222 China
            [4 ]Chinese Glioma Cooperative Group (CGCG), Tianjin, China
            Article
            1271
            10.1186/s12943-020-01271-w
            7597068
            33126881
            6e64b7cf-3f45-4569-8306-b5c55717de8f
            © 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.

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            Oncology & Radiotherapy
            Oncology & Radiotherapy

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