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      MicroRNA-17-5p regulates EMT by targeting vimentin in colorectal cancer

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          Abstract

          Background

          Epithelial–mesenchymal transition (EMT) is the most common cause of death in colorectal cancer (CRC). In this study, we investigated the functional roles of miRNA-17-5p in EMT of CRC cells.

          Methods

          In order to determine if miRNA-17-5p regulated EMT, the precursors and inhibitors of miR-17-5p were transduced into four CRC cells. To evaluate the regulatory mechanism, we performed argonaute 2 (Ago2) immunoprecipitation (IP) and luciferase assay. In addition, we used an intra-splenic injection mouse model of BALB/c nude mice to investigate the metastatic potential of miRNA-17-5p in vivo.

          Results

          The miRNA-17-5p expression was lower in primary CRC tissues with metastasis than in primary CRC tissues without metastasis in our RNA sequencing data of patient tissue. Real-time quantitative PCR revealed that miRNA-17-5p was inversely correlated with that of vimentin in five CRC cell lines. Over-expression of miRNA-17-5p decreased vimentin expression and inhibited cell migration and invasion in both LoVo and HT29 cells. However, inhibition of miRNA-17-5p showed the opposite effect. Ago2 IP and luciferase assay revealed that miRNA-17-5p directly bound to the 3′UTR of VIM mRNA. Furthermore, miRNA-17-5p inhibited the metastasis of CRC into liver in vivo.

          Conclusions

          Our results demonstrated that miRNA-17-5p regulates vimentin expression, thereby regulating metastasis of CRC.

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          Most cited references38

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          Integrative analysis of complex cancer genomics and clinical profiles using the cBioPortal.

          The cBioPortal for Cancer Genomics (http://cbioportal.org) provides a Web resource for exploring, visualizing, and analyzing multidimensional cancer genomics data. The portal reduces molecular profiling data from cancer tissues and cell lines into readily understandable genetic, epigenetic, gene expression, and proteomic events. The query interface combined with customized data storage enables researchers to interactively explore genetic alterations across samples, genes, and pathways and, when available in the underlying data, to link these to clinical outcomes. The portal provides graphical summaries of gene-level data from multiple platforms, network visualization and analysis, survival analysis, patient-centric queries, and software programmatic access. The intuitive Web interface of the portal makes complex cancer genomics profiles accessible to researchers and clinicians without requiring bioinformatics expertise, thus facilitating biological discoveries. Here, we provide a practical guide to the analysis and visualization features of the cBioPortal for Cancer Genomics.
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            The cBio cancer genomics portal: an open platform for exploring multidimensional cancer genomics data.

            The cBio Cancer Genomics Portal (http://cbioportal.org) is an open-access resource for interactive exploration of multidimensional cancer genomics data sets, currently providing access to data from more than 5,000 tumor samples from 20 cancer studies. The cBio Cancer Genomics Portal significantly lowers the barriers between complex genomic data and cancer researchers who want rapid, intuitive, and high-quality access to molecular profiles and clinical attributes from large-scale cancer genomics projects and empowers researchers to translate these rich data sets into biologic insights and clinical applications. © 2012 AACR.
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              MicroRNAs: target recognition and regulatory functions.

              MicroRNAs (miRNAs) are endogenous approximately 23 nt RNAs that play important gene-regulatory roles in animals and plants by pairing to the mRNAs of protein-coding genes to direct their posttranscriptional repression. This review outlines the current understanding of miRNA target recognition in animals and discusses the widespread impact of miRNAs on both the expression and evolution of protein-coding genes.
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                Author and article information

                Contributors
                hyeonhkim@skku.edu
                gscyb@skku.edu
                Journal
                Br J Cancer
                Br. J. Cancer
                British Journal of Cancer
                Nature Publishing Group UK (London )
                0007-0920
                1532-1827
                17 June 2020
                29 September 2020
                : 123
                : 7
                : 1123-1130
                Affiliations
                [1 ]GRID grid.264381.a, ISNI 0000 0001 2181 989X, Department of Health Sciences and Technology, SAIHST, , Sungkyunkwan University, ; Seoul, Republic of Korea
                [2 ]GRID grid.264381.a, ISNI 0000 0001 2181 989X, Sungkyunkwan University School of Medicine, ; Seoul, Republic of Korea
                [3 ]GRID grid.414964.a, ISNI 0000 0001 0640 5613, Institute for Future Medicine, Samsung Medical Center, ; Seoul, Republic of Korea
                [4 ]GRID grid.264381.a, ISNI 0000 0001 2181 989X, Department of Surgery, Samsung Medical Center, , Sungkyunkwan University School of Medicine, ; Seoul, Republic of Korea
                Article
                940
                10.1038/s41416-020-0940-5
                7524803
                32546833
                552d8435-c8bd-4cfc-a7f7-e52f5a345286
                © The Author(s), under exclusive licence to Cancer Research UK 2020

                Note This work is published under the standard license to publish agreement. After 12 months the work will become freely available and the license terms will switch to a Creative Commons Attribution 4.0 International (CC BY 4.0).

                History
                : 10 October 2019
                : 27 April 2020
                : 28 May 2020
                Funding
                Funded by: FundRef https://doi.org/10.13039/501100003725, National Research Foundation of Korea (NRF);
                Award ID: NRF-2017H1A2A1045221
                Award ID: NRF-2016R1A6A3A11933598
                Award ID: NRF-2016R1A6A3A11933598
                Award Recipient :
                Categories
                Article
                Custom metadata
                © Cancer Research UK 2020

                Oncology & Radiotherapy
                metastasis,colorectal cancer
                Oncology & Radiotherapy
                metastasis, colorectal cancer

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