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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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      miR-30a-3p Targets MAD2L1 and Regulates Proliferation of Gastric Cancer Cells

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          Abstract

          Purpose

          This study was done to investigate the inhibition effects of miR-30a-3p on mitotic arrest deficient 2 like 1 (MAD2L1) expression and the proliferation of gastric cancer cells.

          Patients and methods

          Cluster analysis and the TCGA database were used to screen the key genes highly expressed in gastric cancer. Based on the LinkedOmics website, the correlation between the miR-30a-3p and the cell cycle-related target gene MAD2L1 in gastric cancer was analyzed. The mRNA and protein expression levels were detected with the quantitative real-time PCR and Western blot analysis. The cell proliferation and cell cycle were also detected and analyzed.

          Results

          Bioinformatics analysis showed that MAD2L1 was highly expressed in tumor tissues compared with normal tissues. Compared with normal tissues, the miR-30a-3p was significantly decreased in the gastric cancer tissues. Moreover, MAD2L1 was significantly negatively correlated with the miR-30a-3p expression. Furthermore, over-expression of miR-30a-3p decreased the expression of MAD2L1 at the protein level, which inhibited the proliferation of AGS and BGC-823 gastric cancer cells. In addition, the cell cycles of AGS and BGC-823 cells were arrested at the G0/G1 phase.

          Conclusion

          MAD2L1 is a pro-oncogene which is up-regulated in gastric cancer. The miR-30a-3p can down-regulate the MAD2L1 expression, inhibiting the proliferation of gastric cancer cells and affect the cell cycle.

          Most cited references44

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          An abundant class of tiny RNAs with probable regulatory roles in Caenorhabditis elegans.

          N. Lau, L. P. Lim, E G Weinstein … (2001)
          Two small temporal RNAs (stRNAs), lin-4 and let-7, control developmental timing in Caenorhabditis elegans. We find that these two regulatory RNAs are members of a large class of 21- to 24-nucleotide noncoding RNAs, called microRNAs (miRNAs). We report on 55 previously unknown miRNAs in C. elegans. The miRNAs have diverse expression patterns during development: a let-7 paralog is temporally coexpressed with let-7; miRNAs encoded in a single genomic cluster are coexpressed during embryogenesis; and still other miRNAs are expressed constitutively throughout development. Potential orthologs of several of these miRNA genes were identified in Drosophila and human genomes. The abundance of these tiny RNAs, their expression patterns, and their evolutionary conservation imply that, as a class, miRNAs have broad regulatory functions in animals.
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            A double-hexameric MCM2-7 complex is loaded onto origin DNA during licensing of eukaryotic DNA replication.

            Cecile Evrin, Pippa Clarke, Juergen Zech … (2009)
            During pre-replication complex (pre-RC) formation, origin recognition complex (ORC), Cdc6, and Cdt1 cooperatively load the 6-subunit mini chromosome maintenance (MCM2-7) complex onto DNA. Loading of MCM2-7 is a prerequisite for DNA licensing that restricts DNA replication to once per cell cycle. During S phase MCM2-7 functions as part of the replicative helicase but within the pre-RC MCM2-7 is inactive. The organization of replicative DNA helicases before and after loading onto DNA has been studied in bacteria and viruses but not eukaryotes and is of major importance for understanding the MCM2-7 loading mechanism and replisome assembly. Lack of an efficient reconstituted pre-RC system has hindered the detailed mechanistic and structural analysis of MCM2-7 loading for a long time. We have reconstituted Saccharomyces cerevisiae pre-RC formation with purified proteins and showed efficient loading of MCM2-7 onto origin DNA in vitro. MCM2-7 loading was found to be dependent on the presence of all pre-RC proteins, origin DNA, and ATP hydrolysis. The quaternary structure of MCM2-7 changes during pre-RC formation: MCM2-7 before loading is a single hexamer in solution but is transformed into a double-hexamer during pre-RC formation. Using electron microscopy (EM), we observed that loaded MCM2-7 encircles DNA. The loaded MCM2-7 complex can slide on DNA, and sliding is not directional. Our results provide key insights into mechanisms of pre-RC formation and have important implications for understanding the role of the MCM2-7 in establishment of bidirectional replication forks.
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              Mad2 overexpression promotes aneuploidy and tumorigenesis in mice.

              Rocio Sotillo, Eva Hernando, Elena Díaz-Rodríguez … (2007)
              Mad2 is an essential component of the spindle checkpoint that blocks activation of Separase and dissolution of sister chromatids until microtubule attachment to kinetochores is complete. We show here that overexpression of Mad2 in transgenic mice leads to a wide variety of neoplasias, appearance of broken chromosomes, anaphase bridges, and whole-chromosome gains and losses, as well as acceleration of myc-induced lymphomagenesis. Moreover, continued overexpression of Mad2 is not required for tumor maintenance, unlike the majority of oncogenes studied to date. These results demonstrate that transient Mad2 overexpression and chromosome instability can be an important stimulus in the initiation and progression of different cancer subtypes.
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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): 19 December 2019
                Publication date Collection: 2019
                Volume: 12
                Pages: 11313-11324
                Affiliations
                [1 ]Department of Clinical Medicine, Medical College of Yan’an University , Yan’an, Shaanxi 716000, People’s Republic of China
                [2 ]Yan’an Key Laboratory of Chronic Disease Prevention and Research , Yan’an, Shaanxi 716000, People’s Republic of China
                Author notes
                Correspondence: Jing Zhang Department of Clinical Medicine, Medical College of Yan’an University , No. 38, Guanghua Road, Yan’an716000, People’s Republic of ChinaTel +86-911-2650158 Email yadxzj@163.com
                [*]

                These authors contributed equally to this work

                Author information
                http://orcid.org/0000-0003-2281-5297
                Article
                Publisher ID: 222854
                DOI: 10.2147/OTT.S222854
                PMC ID: 6927793
                PubMed ID: 31908496
                SO-VID: 6b6ce8fd-3476-41e1-b33f-5862e907bbf2
                Copyright © © 2019 Wang 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 : 11 July 2019
                Date accepted : 27 November 2019
                Page count
                Figures: 9, References: 51, Pages: 12
                Funding
                This work was supported by the National Natural Science Foundation of China (Grant Nos. 81660492, 81860444 and 81760510), Shaanxi Innovative Talents Promotion Plan-Science and Technology New Star Project (Grant No. 2017KJXX-20), and Scientific Research Plan Projects of Yan’an University (Grant Nos. YDBK2018-49, YD2015-15, YD2019-09, and YDT2016-03).
                Categories
                Subject: Original Research

                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: gastric cancer,bioinformatics analysis,mad2l1,mir-30a-3p,cell proliferation
                Data availability:
                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: gastric cancer, bioinformatics analysis, mad2l1, mir-30a-3p, cell proliferation

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