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    Manganese Superoxide Dismutase Expression Regulates the Switch between an Epithelial and a Mesenchymal-Like Phenotype in Breast Carcinoma

    Access Status
    Fulltext not available
    Authors
    Loo, S.
    Hirpara, J.
    Pandey, V.
    Tan, T.
    Yap, C.
    Lobie, P.
    Thiery, J.
    Goh, B.
    Pervaiz, Shazib
    Clément, M.
    Kumar, Alan Prem
    Date
    2016
    Type
    Journal Article
    
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    Citation
    Loo, S. and Hirpara, J. and Pandey, V. and Tan, T. and Yap, C. and Lobie, P. and Thiery, J. et al. 2016. Manganese Superoxide Dismutase Expression Regulates the Switch between an Epithelial and a Mesenchymal-Like Phenotype in Breast Carcinoma. Antioxidants and Redox Signaling. 25 (6): pp. 283-299.
    Source Title
    Antioxidants and Redox Signaling
    DOI
    10.1089/ars.2015.6524
    ISSN
    1523-0864
    School
    School of Biomedical Sciences
    URI
    http://hdl.handle.net/20.500.11937/51158
    Collection
    • Curtin Research Publications
    Abstract

    Aim: Epithelial-mesenchymal transition (EMT) is characterized by the acquisition of invasive fibroblast-like morphology by epithelial cells that are highly polarized. EMT is recognized as a crucial mechanism in cancer progression and metastasis. In this study, we sought to assess the involvement of manganese superoxide dismutase (MnSOD) during the switch between epithelial-like and mesenchymal-like phenotypes in breast carcinoma. Results: Analysis of breast carcinomas from The Cancer Genome Atlas database revealed strong positive correlation between tumors' EMT score and the expression of MnSOD. This positive correlation between MnSOD and EMT score was significant and consistent across all breast cancer subtypes. Similarly, a positive correlation of EMT score and MnSOD expression was observed in established cell lines derived from breast cancers exhibiting phenotypes ranging from the most epithelial to the most mesenchymal. Interestingly, using phenotypically distinct breast cancer cell lines, we provide evidence that constitutively high or induced expression of MnSOD promotes the EMT-like phenotype by way of a redox milieu predominantly driven by hydrogen peroxide (H2O2). Conversely, gene knockdown of MnSOD results in the reversal of EMT to a mesenchymal-epithelial transition (MET)-like program, which appears to be a function of superoxide (O2-•)-directed signaling. Innovation and Conclusion: These data underscore the involvement of MnSOD in regulating the switch between the EMT and MET-associated phenotype by influencing cellular redox environment via its effect on the intracellular ratio between O2-• and H2O2. Strategies to manipulate MnSOD expression and/or the cellular redox milieu vis-a-vis O2-•:H2O2 could have potential therapeutic implications.

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