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The Role of Drebrin in Cancer Cell Invasion

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Book cover Drebrin

Part of the book series: Advances in Experimental Medicine and Biology ((AEMB,volume 1006))

Abstract

Cancer progression is characterized by the capacity of malignant cells to exploit an innate migratory ability in order to invade adjacent tissues, enter the vasculature and eventually metastasize to secondary organs. It is this spread of cancer cells that is the major cause of death in cancer patients. Understanding the basic biology of how cancer cells generate an invasive phenotype will be crucial to the identification of drug targets with the aim of impeding tumour dissemination. Ten years on from its initial description in neuronal cells, drebrin expression was found in a wide variety of non-neuronal cells that importantly included cancer cell lines. Since then mounting evidence suggests that drebrin may be a key player in the advancement of several diverse cancer types where its expression is frequently upregulated. Cancer cell motility and invasion are crucial elements in the metastatic cascade and involve dramatic changes in cellular morphology that are associated with dynamic remodelling of the cytoskeleton. Interestingly, it now appears that drebrin could deliver this role during cancer development.

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Authors and Affiliations

  1. MRC Centre for Developmental Neurobiology, New Hunt’s House, King’s College London, Guy’s Campus, London, SE1 1UL, UK

    Anna E. Dart & Phillip R. Gordon-Weeks

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  1. Anna E. Dart
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  2. Phillip R. Gordon-Weeks
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Correspondence to Anna E. Dart .

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Editors and Affiliations

  1. Department of Neurobiology and Behavior, Gunma University Graduate School of Medicine, Maebashi, Gunma, Japan

    Tomoaki Shirao

  2. Laboratory of Chemical Pharmacology, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Tokyo, Japan

    Yuko Sekino

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Dart, A.E., Gordon-Weeks, P.R. (2017). The Role of Drebrin in Cancer Cell Invasion. In: Shirao, T., Sekino, Y. (eds) Drebrin. Advances in Experimental Medicine and Biology, vol 1006. Springer, Tokyo. https://doi.org/10.1007/978-4-431-56550-5_23

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