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    Curcumin induces apoptosis-independent death in oesophageal cancer cells.

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    Authors
    O'Sullivan-Coyne, G
    O'Sullivan, G C
    O'Donovan, T R
    Piwocka, K
    McKenna, S L
    Affiliation
    Leslie C. Quick Laboratory, Cork Cancer Research Centre, BioSciences Institute,, University College Cork and Mercy University Hospital, Cork, Ireland.
    Issue Date
    2012-01-31T16:39:15Z
    MeSH
    Antineoplastic Agents/*pharmacology
    Apoptosis/*drug effects
    Autophagy/drug effects
    Caspase 3/metabolism
    Cell Cycle/drug effects
    Cell Line, Tumor
    Cell Survival/drug effects
    Curcumin/*pharmacology
    Cyclin B/metabolism
    Cyclin B1
    Esophageal Neoplasms/*drug therapy/pathology
    Humans
    Mitotic Index
    Proteasome Endopeptidase Complex/physiology
    Ubiquitin/metabolism
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    Citation
    Br J Cancer. 2009 Nov 3;101(9):1585-95. Epub 2009 Oct 6.
    Journal
    British journal of cancer
    URI
    http://hdl.handle.net/10147/206267
    DOI
    10.1038/sj.bjc.6605308
    PubMed ID
    19809435
    Abstract
    BACKGROUND: Oesophageal cancer incidence is increasing and survival rates remain extremely poor. Natural agents with potential for chemoprevention include the phytochemical curcumin (diferuloylmethane). We have examined the effects of curcumin on a panel of oesophageal cancer cell lines. METHODS: MTT (3-(4,5-dimethyldiazol-2-yl)-2,5 diphenyl tetrazolium bromide) assays and propidium iodide staining were used to assess viability and DNA content, respectively. Mitotic catastrophe (MC), apoptosis and autophagy were defined by both morphological criteria and markers such as MPM-2, caspase 3 cleavage and monodansylcadaverine (MDC) staining. Cyclin B and poly-ubiquitinated proteins were assessed by western blotting. RESULTS: Curcumin treatment reduces viability of all cell lines within 24 h of treatment in a 5-50 muM range. Cytotoxicity is associated with accumulation in G2/M cell-cycle phases and distinct chromatin morphology, consistent with MC. Caspase-3 activation was detected in two out of four cell lines, but was a minor event. The addition of a caspase inhibitor zVAD had a marginal or no effect on cell viability, indicating predominance of a non-apoptotic form of cell death. In two cell lines, features of both MC and autophagy were apparent. Curcumin-responsive cells were found to accumulate poly-ubiquitinated proteins and cyclin B, consistent with a disturbance of the ubiquitin-proteasome system. This effect on a key cell-cycle checkpoint regulator may be responsible for the mitotic disturbances and consequent cytotoxicity of this drug. CONCLUSION: Curcumin can induce cell death by a mechanism that is not reliant on apoptosis induction, and thus represents a promising anticancer agent for prevention and treatment of oesophageal cancer.
    Language
    eng
    ISSN
    1532-1827 (Electronic)
    0007-0920 (Linking)
    ae974a485f413a2113503eed53cd6c53
    10.1038/sj.bjc.6605308
    Scopus Count
    Collections
    Mercy University Hospital

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