10
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Molecular crosstalk between cancer and neurodegenerative diseases

      review-article

      Read this article at

      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

          The progression of cancers and neurodegenerative disorders is largely defined by a set of molecular determinants that are either complementarily deregulated, or share remarkably overlapping functional pathways. A large number of such molecules have been demonstrated to be involved in the progression of both diseases. In this review, we particularly discuss our current knowledge on p53, cyclin D, cyclin E, cyclin F, Pin1 and protein phosphatase 2A, and their implications in the shared or distinct pathways that lead to cancers or neurodegenerative diseases. In addition, we focus on the inter-dependent regulation of brain cancers and neurodegeneration, mediated by intercellular communication between tumor and neuronal cells in the brain through the extracellular microenvironment. Finally, we shed light on the therapeutic perspectives for the treatment of both cancer and neurodegenerative disorders.

          Related collections

          Most cited references257

          • Record: found
          • Abstract: not found
          • Article: not found

          Cancer. p53, guardian of the genome.

          D P Lane (1992)
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Inflammation and cancer: advances and new agents.

            Tumour-promoting inflammation is considered one of the enabling characteristics of cancer development. Chronic inflammatory disease increases the risk of some cancers, and strong epidemiological evidence exists that NSAIDs, particularly aspirin, are powerful chemopreventive agents. Tumour microenvironments contain many different inflammatory cells and mediators; targeting these factors in genetic, transplantable and inducible murine models of cancer substantially reduces the development, growth and spread of disease. Thus, this complex network of inflammation offers targets for prevention and treatment of malignant disease. Much potential exists in this area for novel cancer prevention and treatment strategies, although clinical research to support targeting of cancer-related inflammation and innate immunity in patients with advanced-stage cancer remains in its infancy. Following the initial successes of immunotherapies that modulate the adaptive immune system, we assert that inflammation and innate immunity are important targets in patients with cancer on the basis of extensive preclinical and epidemiological data. The adaptive immune response is heavily dependent on innate immunity, therefore, inhibiting some of the tumour-promoting immunosuppressive actions of the innate immune system might enhance the potential of immunotherapies that activate a nascent antitumour response.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              SKP1 connects cell cycle regulators to the ubiquitin proteolysis machinery through a novel motif, the F-box.

              We have identified the yeast and human homologs of the SKP1 gene as a suppressor of cdc4 mutants and as a cyclin F-binding protein. Skp1p indirectly binds cyclin A/Cdk2 through Skp2p, and directly binds Skp2p, cyclin F, and Cdc4p through a novel structural motif called the F-box. SKP1 is required for ubiquitin-mediated proteolysis of Cin2p, Clb5p, and the Cdk inhibitor Sic1p, and provides a link between these molecules and the proteolysis machinery. A large number of proteins contain the F-box motif and are thereby implicated in the ubiquitin pathway. Different skp1 mutants arrest cells in either G1 or G2, suggesting a connection between regulation of proteolysis in different stages of the cycle.
                Bookmark

                Author and article information

                Contributors
                mikyoungpark7@gmail.com , mpark@kist.re.kr
                Journal
                Cell Mol Life Sci
                Cell. Mol. Life Sci
                Cellular and Molecular Life Sciences
                Springer International Publishing (Cham )
                1420-682X
                1420-9071
                28 December 2019
                28 December 2019
                2020
                : 77
                : 14
                : 2659-2680
                Affiliations
                [1 ]GRID grid.35541.36, ISNI 0000000121053345, Center for Functional Connectomics, Brain Science Institute, , Korea Institute of Science and Technology, ; Seoul, 02792 South Korea
                [2 ]GRID grid.412786.e, ISNI 0000 0004 1791 8264, Department of Neuroscience, , Korea University of Science and Technology, ; Daejeon, 34113 South Korea
                [3 ]GRID grid.35541.36, ISNI 0000000121053345, Center for Neuroscience, Brain Science Institute, , Korea Institute of Science and Technology, ; Seoul, 02792 South Korea
                Author information
                http://orcid.org/0000-0002-5589-0624
                Article
                3428
                10.1007/s00018-019-03428-3
                7326806
                31884567
                be9f5ce0-df2e-468a-a59e-6e205fb4805d
                © The Author(s) 2019

                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
                : 18 September 2019
                : 11 December 2019
                : 13 December 2019
                Funding
                Funded by: the Original Technology Research Program for Brain Science of the National Research Foundation of Korea
                Award ID: 2018M3C7A1021848
                Award Recipient :
                Categories
                Review
                Custom metadata
                © Springer Nature Switzerland AG 2020

                Molecular biology
                age-related diseases,cell death,cell survival,redox system,glioma,neurotoxicity
                Molecular biology
                age-related diseases, cell death, cell survival, redox system, glioma, neurotoxicity

                Comments

                Comment on this article