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    Mitochondrial fission as a driver of stemness in tumor cells: mDIVI1 inhibits mitochondrial function, cell migration and cancer stem cell (CSC) signalling.

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    Authors
    Peiris-Pagès, Maria
    Bonuccelli, Gloria
    Sotgia, Federica
    Lisanti, Michael P
    Affiliation
    Clinical and Experimental Pharmacology Group, Cancer Research UK Manchester Institute, University of Manchester, Manchester, UK
    Issue Date
    2018-03-02
    
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    Show full item record
    Abstract
    Mitochondria are dynamic organelles frequently undergoing fission and fusion events to maintain their integrity, bioenergetics and spatial distribution, which is fundamental to the processes of cell survival. Disruption in mitochondrial dynamics plays a role in cancer. Therefore, proteins involved in regulating mitochondrial dynamics are potential targets for treatment. mDIVI1 is an inhibitor of the mitochondrial fission protein DRP1, which induces i) mitochondrial oxidative stress and ii) effectively reduces mitochondrial metabolism. We show here that mDIVI1 is able to inhibit 3D tumorsphere forming capacity, cell migration and stemness-related signalling in breast cancer cells, indicating that mDIVI1 can potentially be used for the therapeutic elimination of cancer stem cells (CSCs).
    Citation
    Mitochondrial fission as a driver of stemness in tumor cells: mDIVI1 inhibits mitochondrial function, cell migration and cancer stem cell (CSC) signalling. 2018, 9(17): 13254-13275 Oncotarget
    Journal
    Oncotarget
    URI
    http://hdl.handle.net/10541/620988
    DOI
    10.18632/oncotarget.24285
    PubMed ID
    29568355
    Type
    Article
    Language
    en
    ISSN
    1949-2553
    ae974a485f413a2113503eed53cd6c53
    10.18632/oncotarget.24285
    Scopus Count
    Collections
    All Paterson Institute for Cancer Research

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