24
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Zinc finger proteins in cancer progression

      review-article
      ,
      Journal of Biomedical Science
      BioMed Central
      Zinc finger protein, Transcription factor, Cancer progression

      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

          Zinc finger proteins are the largest transcription factor family in human genome. The diverse combinations and functions of zinc finger motifs make zinc finger proteins versatile in biological processes, including development, differentiation, metabolism and autophagy. Over the last few decades, increasing evidence reveals the potential roles of zinc finger proteins in cancer progression. However, the underlying mechanisms of zinc finger proteins in cancer progression vary in different cancer types and even in the same cancer type under different types of stress. Here, we discuss general mechanisms of zinc finger proteins in transcription regulation and summarize recent studies on zinc finger proteins in cancer progression. In this review, we also emphasize the importance of further investigations in elucidating the underlying mechanisms of zinc finger proteins in cancer progression.

          Related collections

          Most cited references88

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

          Structural classification of zinc fingers: survey and summary.

          S Krishna (2003)
          Zinc fingers are small protein domains in which zinc plays a structural role contributing to the stability of the domain. Zinc fingers are structurally diverse and are present among proteins that perform a broad range of functions in various cellular processes, such as replication and repair, transcription and translation, metabolism and signaling, cell proliferation and apoptosis. Zinc fingers typically function as interaction modules and bind to a wide variety of compounds, such as nucleic acids, proteins and small molecules. Here we present a comprehensive classification of zinc finger spatial structures. We find that each available zinc finger structure can be placed into one of eight fold groups that we define based on the structural properties in the vicinity of the zinc-binding site. Three of these fold groups comprise the majority of zinc fingers, namely, C2H2-like finger, treble clef finger and the zinc ribbon. Evolutionary relatedness of proteins within fold groups is not implied, but each group is divided into families of potential homologs. We compare our classification to existing groupings of zinc fingers and find that we define more encompassing fold groups, which bring together proteins whose similarities have previously remained unappreciated. We analyze functional properties of different zinc fingers and overlay them onto our classification. The classification helps in understanding the relationship between the structure, function and evolutionary history of these domains. The results are available as an online database of zinc finger structures.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Coordinated histone modifications mediated by a CtBP co-repressor complex.

            The transcriptional co-repressor CtBP (C-terminal binding protein) is implicated in tumorigenesis because it is targeted by the adenovirus E1A protein during oncogenic transformation. Genetic studies have also identified a crucial function for CtBP in animal development. CtBP is recruited to DNA by transcription factors that contain a PXDLS motif, but the detailed molecular events after the recruitment of CtBP to DNA and the mechanism of CtBP function in tumorigenesis are largely unknown. Here we report the identification of a CtBP complex that contains the essential components for both gene targeting and coordinated histone modifications, allowing for the effective repression of genes targeted by CtBP. Inhibiting the expression of CtBP and its associated histone-modifying activities by RNA-mediated interference resulted in alterations of histone modifications at the promoter of the tumour invasion suppressor gene E-cadherin and increased promoter activity in a reporter assay. These findings identify a molecular mechanism by which CtBP mediates transcriptional repression and provide insight into CtBP participation in oncogenesis.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: found
              Is Open Access

              ZEB1 turns into a transcriptional activator by interacting with YAP1 in aggressive cancer types

              Early dissemination, metastasis and therapy resistance are central hallmarks of aggressive cancer types and the leading cause of cancer-associated deaths. The EMT-inducing transcriptional repressor ZEB1 is a crucial stimulator of these processes, particularly by coupling the activation of cellular motility with stemness and survival properties. ZEB1 expression is associated with aggressive behaviour in many tumour types, but the potent effects cannot be solely explained by its proven function as a transcriptional repressor of epithelial genes. Here we describe a direct interaction of ZEB1 with the Hippo pathway effector YAP, but notably not with its paralogue TAZ. In consequence, ZEB1 switches its function to a transcriptional co-activator of a ‘common ZEB1/YAP target gene set', thereby linking two pathways with similar cancer promoting effects. This gene set is a predictor of poor survival, therapy resistance and increased metastatic risk in breast cancer, indicating the clinical relevance of our findings.
                Bookmark

                Author and article information

                Contributors
                +886-6-2353535 ext.5476 , jayujen1021@gmail.com
                +886-6-2353535 ext.5502 , ycw5798@mail.ncku.edu.tw
                Journal
                J Biomed Sci
                J. Biomed. Sci
                Journal of Biomedical Science
                BioMed Central (London )
                1021-7770
                1423-0127
                13 July 2016
                13 July 2016
                2016
                : 23
                : 53
                Affiliations
                [ ]Department of Pharmacology, College of Medicine, National Cheng Kung University, No.1, University Road, Tainan, 70101 Taiwan, Republic of China
                [ ]Department of Basic Medical Sciences, College of Medicine, National Cheng Kung University, No.1, University Road, Tainan, 70101 Taiwan, Republic of China
                Article
                269
                10.1186/s12929-016-0269-9
                4944467
                27411336
                0cf97e5b-551b-41c1-9955-6097bc0bf301
                © The Author(s). 2016

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. 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.

                History
                : 12 May 2016
                : 1 July 2016
                Funding
                Funded by: The Aim for the Top University Project
                Award ID: D105-35A07
                Award Recipient :
                Funded by: FundRef http://dx.doi.org/10.13039/501100004663, Ministry of Science and Technology, Taiwan;
                Award ID: 104-2627-B-006-001
                Award Recipient :
                Funded by: FundRef http://dx.doi.org/10.13039/100008903, Ministry of Health and Welfare;
                Award ID: 105-TDU-B-211-124-003
                Award Recipient :
                Categories
                Review
                Custom metadata
                © The Author(s) 2016

                Molecular medicine
                zinc finger protein,transcription factor,cancer progression
                Molecular medicine
                zinc finger protein, transcription factor, cancer progression

                Comments

                Comment on this article