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    The cellular chloride channels CLIC1 and CLIC4 contribute to virus-mediated cell motility

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    Publication date
    2018-03
    Author
    Stakaityte, G.
    Nwogu, N.
    Lippiat, J.D.
    Blair, G.E.
    Poterlowicz, Krzysztof
    Boyne, James R.
    Macdonald, A.
    Mankouri, J.
    Whitehouse, A.
    Keyword
    Cell motility; Cell migration; Channel activation; Chloride channel; Viral protein
    Rights
    © 2018 by The American Society for Biochemistry and Molecular Biology, Inc. Reproduced in accordance with the publisher's self-archiving policy. Author's Choice—Final version free via Creative Commons CC-BY license.
    Peer-Reviewed
    Yes
    
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    Abstract
    Ion channels regulate many aspects of cell physiology, including cell proliferation, motility, and migration, and aberrant expression and activity of ion channels is associated with various stages of tumor development, with K+ and Cl- channels now being considered the most active during tumorigenesis. Accordingly, emerging in vitro and preclinical studies have revealed that pharmacological manipulation of ion channel activity offers protection against several cancers. Merkel cell polyomavirus (MCPyV) is a major cause of Merkel cell carcinoma (MCC), primarily due to the expression of two early regulatory proteins termed small and large tumour antigens (ST and LT, respectively). Several molecular mechanisms have been attributed to MCPyVmediated cancer formation but thus far, no studies have investigated any potential link to cellular ion channels. Here we demonstrate that Cl- channel modulation can reduce MCPyV STinduced cell motility and invasiveness. Proteomic analysis revealed that MCPyV ST upregulates two Cl- channels; CLIC1 and CLIC4, which when silenced, inhibit MCPyV STinduced motility and invasiveness, implicating their function as critical to MCPyV-induced metastatic processes. Consistent with these data, we confirmed that CLIC1 and CLIC4 are upregulated in primary MCPyV-positive MCC patient samples. We therefore, for the first time, implicate cellular ion channels as a key host cell factor contributing to virus-mediated cellular transformation. Given the intense interest in ion channel modulating drugs for human disease, this highlights CLIC1 and CLIC4 activity as potential targets for MCPyV-induced MCC.
    URI
    http://hdl.handle.net/10454/15061
    Version
    Accepted Manuscript
    Citation
    Stakaityte G, Nwogu N, Lippiat JD et al (2018) The cellular chloride channels CLIC1 and CLIC4 contribute to virus-mediated cell motility. Journal of Biological Chemistry. 293(12): 4582-4590.
    Link to publisher’s version
    http://dx.doi.org/10.1074/jbc.RA117.001343
    Type
    Article
    Collections
    Life Sciences Publications

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