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    Differential effects of chemotherapeutic drugs versus the MDM-2 antagonist Nutlin-3 on cell cycle progression and induction of apoptosis in SKW6.4 lymphoblastoid B-cells

    Access Status
    Fulltext not available
    Authors
    Barbarotto, E.
    Corallini, F.
    Rimondi, E.
    Fadda, R.
    Mischiati, C.
    Grill, V.
    Vaccarezza, Mauro
    Celeghini, C.
    Date
    2008
    Type
    Journal Article
    
    Metadata
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    Citation
    Barbarotto, E. and Corallini, F. and Rimondi, E. and Fadda, R. and Mischiati, C. and Grill, V. and Vaccarezza, M. et al. 2008. Differential effects of chemotherapeutic drugs versus the MDM-2 antagonist Nutlin-3 on cell cycle progression and induction of apoptosis in SKW6.4 lymphoblastoid B-cells. Journal of Cellular Biochemistry. 104 (2): pp. 595-605.
    Source Title
    Journal of Cellular Biochemistry
    DOI
    10.1002/jcb.21649
    ISSN
    0730-2312
    School
    School of Biomedical Sciences
    URI
    http://hdl.handle.net/20.500.11937/3008
    Collection
    • Curtin Research Publications
    Abstract

    We have compared the cytotoxic/cytostatic responses of the SKW6.4 lymphoblastoid B-cells to the alkylating agent chlorambucil, the purine analog fludarabine, the non-genotoxic activator of the p53 pathway, Nutlin-3, used alone or in association with the death-inducing ligand recombinant TRAIL. Exposure to chlorambucil, fludarabine, and Nutlin-3 induced p53 accumulation and variably affected cell cycle progression in SKW6.4 lymphoblastoid cells. In particular, chlorambucil induced cell cycle accumulation at the G2/M checkpoint; Nutlin-3 induced early cell cycle arrest at the G1/S checkpoint, while fludarabine showed an intermediate behavior. On the other hand, recombinant TRAIL alone did not affect cell cycle progression but induced a rapid increase of apoptosis. Analysis of the gene expression profile of the p53-transcriptional targets showed distinct features between chlorambucil, Nutlin-3 and fludarabine, which likely account for their differential effect on cell cycle in SKW6.4 cells. In particular, chlorambucil upregulated the steady-state mRNA expression of SFN/14-3-3s, a gene involved in G2/M cell cycle arrest. Of note, all agonists upregulated TRAIL-R2 expression in SKW6.4 cells both at the mRNA and protein levels. Consistently, pretreatment with chlorambucil, fludarabine and Nutlin-3 enhanced SKW6.4 sensitivity to TRAIL-mediated apoptosis. © 2007 Wiley-Liss, Inc.

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