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      Mechanisms of Neural Crest Migration

      Author(s): 1 , 1
      Publication date Created:
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      Journal: Annual Review of Genetics
      Publisher: Annual Reviews

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          Abstract

          Neural crest cells are a transient embryonic cell population that migrate collectively to various locations throughout the embryo to contribute a number of cell types to several organs. After induction, the neural crest delaminates and undergoes an epithelial-to-mesenchymal transition before migrating through intricate yet characteristic paths. The neural crest exhibits a variety of migratory behaviors ranging from sheet-like mass migration in the cephalic regions to chain migration in the trunk. During their journey, neural crest cells rely on a range of signals both from their environment and within the migrating population for navigating through the embryo as a collective. Here we review these interactions and mechanisms, including chemotactic cues of neural crest cells’ migration.

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          Epithelial-mesenchymal transitions in development and disease.

          Jean Paul Thiery, Hervé Acloque, Ruby Y J Huang … (2009)
          The epithelial to mesenchymal transition (EMT) plays crucial roles in the formation of the body plan and in the differentiation of multiple tissues and organs. EMT also contributes to tissue repair, but it can adversely cause organ fibrosis and promote carcinoma progression through a variety of mechanisms. EMT endows cells with migratory and invasive properties, induces stem cell properties, prevents apoptosis and senescence, and contributes to immunosuppression. Thus, the mesenchymal state is associated with the capacity of cells to migrate to distant organs and maintain stemness, allowing their subsequent differentiation into multiple cell types during development and the initiation of metastasis.
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            Tumour microenvironment - opinion: validating matrix metalloproteinases as drug targets and anti-targets for cancer therapy.

            Christopher Overall, Oded Kleifeld (2006)
            The matrix metalloproteinases (MMPs) mediate homeostasis of the extracellular environment. They have multiple signalling activities that are commonly altered during tumorigenesis and that might serve as intervention points for anticancer drugs. However, there are many criteria to consider in validating MMPs as drug targets and for the development of MMP inhibitors. The inhibition of some MMPs could have pro-tumorigenic effects (making them anti-targets), counterbalancing the benefits of target inhibition. These effects might partially account for the failure of MMP inhibitors in clinical trials. What are the major challenges in MMP target validation and MMP-inhibitor-drug development?
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              A gene regulatory network orchestrates neural crest formation.

              Tatjana Sauka-Spengler, Marianne Bronner-Fraser (2008)
              The neural crest is a multipotent, migratory cell population that is unique to vertebrate embryos and gives rise to many derivatives, ranging from the peripheral nervous system to the craniofacial skeleton and pigment cells. A multimodule gene regulatory network mediates the complex process of neural crest formation, which involves the early induction and maintenance of the precursor pool, emigration of the neural crest progenitors from the neural tube via an epithelial to mesenchymal transition, migration of progenitor cells along distinct pathways and overt differentiation into diverse cell types. Here, we review our current understanding of these processes and discuss the molecular players that are involved in the neural crest gene regulatory network.
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                Author and article information

                Journal
                Title: Annual Review of Genetics
                Abbreviated Title: Annu. Rev. Genet.
                Publisher: Annual Reviews
                ISSN (Print): 0066-4197
                ISSN (Electronic): 1545-2948
                Publication date Created: November 23 2018
                Publication date (Print): November 23 2018
                Volume: 52
                Issue: 1
                Pages: 43-63
                Affiliations
                [1 ]Department of Cell and Developmental Biology, University College London, London WC1E 6BT, United Kingdom;
                Article
                DOI: 10.1146/annurev-genet-120417-031559
                PubMed ID: 30476447
                SO-VID: 20af4242-cb8c-4787-974a-2035c75f2bc6
                Copyright © © 2018
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