For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
9
views
23
references
 Top references
cited by
3
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
0 collections
    0
    shares
      400
      similar
       All similar
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Effect of Nanog overexpression on the metastatic potential of a mouse melanoma cell line B16-BL6

      research-article

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Nanog, a marker and regulator of the undifferentiated state in embryonic stem cells were anticipated to be an effective enhancer of cancer metastasis. We have developed a Nanog overexpressing mouse melanoma cell line B16-BL6 (BL6). BL6 was well recognized as a cell line with a high metastatic potential. In vitro tests revealed the enhancement of cell proliferation, wound healing activity, and matrix metalloproteinase 9 (MMP9) activity. Nanog-induced up- or down-regulated genes were comprehensively analyzed by transcriptome sequencing using Nanog +BL6 and wild-type BL6. Principally, up-regulated genes were involved in vesicle-aided glucose transport and oxidative phosphorylation, while down-regulated genes were associated with immunosuppression and apoptosis. A marked finding was that TGF-β1 was down-regulated, because TGF-β1 has been well discussed about its suppressive/progressive dual role in cancer. In vivo test showed that the number and volume of metastatic colonies of BL6 to lung were as high as 115 colonies/lung and 5.6 mm 3/lung. Under this condition, Nanog overexpression caused a progressive effect (150 colonies/lung, p = 0.25; 9.2 mm 3/lung, p = 0.13) rather than a suppressive effect on the metastasis. In this study, the effectiveness of Nanog overexpression in enhancing the metastatic potential of melanoma cell lines has been demonstrated for the first time.

          Supplementary Information

          The online version contains supplementary material available at 10.1007/s11010-021-04110-8.

          Related collections

          Most cited references23

          • Record: found
          • Abstract: found
          • Article: found
          Is Open Access

          KEGG for linking genomes to life and the environment

          Minoru Kanehisa, Michihiro Araki, Susumu Goto … (2008)
          KEGG (http://www.genome.jp/kegg/) is a database of biological systems that integrates genomic, chemical and systemic functional information. KEGG provides a reference knowledge base for linking genomes to life through the process of PATHWAY mapping, which is to map, for example, a genomic or transcriptomic content of genes to KEGG reference pathways to infer systemic behaviors of the cell or the organism. In addition, KEGG provides a reference knowledge base for linking genomes to the environment, such as for the analysis of drug-target relationships, through the process of BRITE mapping. KEGG BRITE is an ontology database representing functional hierarchies of various biological objects, including molecules, cells, organisms, diseases and drugs, as well as relationships among them. KEGG PATHWAY is now supplemented with a new global map of metabolic pathways, which is essentially a combined map of about 120 existing pathway maps. In addition, smaller pathway modules are defined and stored in KEGG MODULE that also contains other functional units and complexes. The KEGG resource is being expanded to suit the needs for practical applications. KEGG DRUG contains all approved drugs in the US and Japan, and KEGG DISEASE is a new database linking disease genes, pathways, drugs and diagnostic markers.
          Article 0 comments Cited 974 times – based on 0 reviews     Review now
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Stem cells, cancer, and cancer stem cells.

            T Reya, S Morrison, M F Clarke … (2001)
            Stem cell biology has come of age. Unequivocal proof that stem cells exist in the haematopoietic system has given way to the prospective isolation of several tissue-specific stem and progenitor cells, the initial delineation of their properties and expressed genetic programmes, and the beginnings of their utility in regenerative medicine. Perhaps the most important and useful property of stem cells is that of self-renewal. Through this property, striking parallels can be found between stem cells and cancer cells: tumours may often originate from the transformation of normal stem cells, similar signalling pathways may regulate self-renewal in stem cells and cancer cells, and cancer cells may include 'cancer stem cells' - rare cells with indefinite potential for self-renewal that drive tumorigenesis.
            Article 0 comments Cited 704 times – based on 0 reviews     Review now
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Pluripotency governed by Sox2 via regulation of Oct3/4 expression in mouse embryonic stem cells.

              Shinji Masui, Yuhki Nakatake, Yayoi Toyooka … (2007)
              The pluripotency of embryonic stem (ES) cells is thought to be maintained by a few key transcription factors, including Oct3/4 and Sox2. The function of Oct3/4 in ES cells has been extensively characterized, but that of Sox2 has yet to be determined. Sox2 can act synergistically with Oct3/4 in vitro to activate Oct-Sox enhancers, which regulate the expression of pluripotent stem cell-specific genes, including Nanog, Oct3/4 and Sox2 itself. These findings suggest that Sox2 is required by ES cells for its Oct-Sox enhancer activity. Using inducible Sox2-null mouse ES cells, we show that Sox2 is dispensable for the activation of these Oct-Sox enhancers. In contrast, we demonstrate that Sox2 is necessary for regulating multiple transcription factors that affect Oct3/4 expression and that the forced expression of Oct3/4 rescues the pluripotency of Sox2-null ES cells. These results indicate that the essential function of Sox2 is to stabilize ES cells in a pluripotent state by maintaining the requisite level of Oct3/4 expression.
              Article 0 comments Cited 316 times – based on 0 reviews     Review now
                Bookmark
                All references

                Author and article information

                Contributors
                Mikako Saito:
                ORCID: http://orcid.org/0000-0002-7941-6839
                mikako@cc.tuat.ac.jp
                Journal
                Journal ID (nlm-ta): Mol Cell Biochem
                Journal ID (iso-abbrev): Mol Cell Biochem
                Title: Molecular and Cellular Biochemistry
                Publisher: Springer US (New York )
                ISSN (Print): 0300-8177
                ISSN (Electronic): 1573-4919
                Publication date (Electronic): 4 March 2021
                Publication date PMC-release: 4 March 2021
                Publication date (Print): 2021
                Volume: 476
                Issue: 7
                Pages: 2651-2661
                Affiliations
                GRID grid.136594.c, Department of Biotechnology and Life Science, , Tokyo University of Agriculture and Technology, ; 2-24-16, Naka-cho, Koganei, Tokyo 184-8588 Japan
                Author information
                http://orcid.org/0000-0002-7941-6839
                Article
                Publisher ID: 4110
                DOI: 10.1007/s11010-021-04110-8
                PMC ID: 8192392
                PubMed ID: 33665763
                SO-VID: a48733ea-401b-44e3-aab9-20e11b52fd87
                Copyright © © The Author(s) 2021
                License:

                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/.

                History
                Date received : 17 July 2020
                Date accepted : 12 February 2021
                Categories
                Subject: Article
                Custom metadata
                issue-copyright-statement © Springer Science+Business Media, LLC, part of Springer Nature 2021

                ScienceOpen disciplines: Biochemistry
                Keywords: nanog,undifferentiated state,mouse melanoma,metastasis,mmp9
                Data availability:
                ScienceOpen disciplines: Biochemistry
                Keywords: nanog, undifferentiated state, mouse melanoma, metastasis, mmp9

                Comments

                Comment on this article

                scite_

                Similar content400

                See all similar

                Cited by3

                See all cited by

                Most referenced authors306

                See all reference authors