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    Dextran-Catechin: An anticancer chemically-modified natural compound targeting copper that attenuates neuroblastoma growth.

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    Author
    Vittorio, O; Brandl, M; Cirillo, G; Kimpton, K; Hinde, E; Gaus, K; Yee, E; Kumar, N; Duong, H; Fleming, C; ...
    Date
    2016-07-26
    Source Title
    Oncotarget
    Publisher
    Impact Journals, LLC
    University of Melbourne Author/s
    Hinde, Elizabeth
    Affiliation
    School of Physics
    Metadata
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    Document Type
    Journal Article
    Citations
    Vittorio, O., Brandl, M., Cirillo, G., Kimpton, K., Hinde, E., Gaus, K., Yee, E., Kumar, N., Duong, H., Fleming, C., Haber, M., Norris, M., Boyer, C. & Kavallaris, M. (2016). Dextran-Catechin: An anticancer chemically-modified natural compound targeting copper that attenuates neuroblastoma growth.. Oncotarget, 7 (30), pp.47479-47493. https://doi.org/10.18632/oncotarget.10201.
    Access Status
    Open Access
    URI
    http://hdl.handle.net/11343/256848
    DOI
    10.18632/oncotarget.10201
    Open Access at PMC
    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5216955
    Abstract
    Neuroblastoma is frequently diagnosed at advanced stage disease and treatment includes high dose chemotherapy and surgery. Despite the use of aggressive therapy survival rates are poor and children that survive their disease experience long term side effects from their treatment, highlighting the need for effective and less toxic therapies. Catechin is a natural polyphenol with anti-cancer properties and limited side effects, however its mechanism of action is unknown. Here we report that Dextran-Catechin, a conjugated form of catechin that increases serum stability, is preferentially and markedly active against neuroblastoma cells having high levels of intracellular copper, without affecting non-malignant cells. Copper transporter 1 (CTR1) is the main transporter of copper in mammalian cells and it is upregulated in neuroblastoma. Functional studies showed that depletion of CTR1 expression reduced intracellular copper levels and led to a decrease in neuroblastoma cell sensitivity to Dextran-Catechin, implicating copper in the activity of this compound. Mechanistically, Dextran-Catechin was found to react with copper, inducing oxidative stress and decreasing glutathione levels, an intracellular antioxidant and regulator of copper homeostasis. In vivo, Dextran-Catechin significantly attenuated tumour growth in human xenograft and syngeneic models of neuroblastoma. Thus, Dextran-Catechin targets copper, inhibits tumour growth, and may be valuable in the treatment of aggressive neuroblastoma and other cancers dependent on copper for their growth.

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