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  • Title: c-Myc-dependent etoposide-induced apoptosis involves activation of Bax and caspases, and PKCdelta signaling.
    Author: Albihn A, Lovén J, Ohlsson J, Osorio LM, Henriksson M.
    Journal: J Cell Biochem; 2006 Aug 15; 98(6):1597-614. PubMed ID: 16572399.
    Abstract:
    The c-Myc transcription factor is a key regulator of cell proliferation, differentiation, and apoptosis. While deregulation of myc induces programmed cell death, defects in the apoptotic program facilitate Myc-driven tumor development. We have treated c-Myc inducible mouse cells and rat fibroblasts with different c-myc status with cytotoxic drugs to explore the effect of c-Myc on drug-induced apoptosis. We found that c-Myc overexpression potentiated etoposide-, doxorubicin-, and cisplatin-induced cell death in mouse fibroblasts. In addition, these drugs provoked a strong apoptotic response in c-Myc-expressing cells, but a weak apoptosis in c-myc null Rat1 cells. In contrast, staurosporine-induced apoptosis was c-Myc-independent, confirming a functional apoptotic pathway in c-myc null cells. Apoptosis was paralleled by c-Myc-dependent Bax-activation after etoposide and doxorubicin treatment, but not after cisplatin administration. All three drugs induced higher caspase activation in c-Myc expressing cells than in c-myc null cells. Furthermore, etoposide treatment of c-Myc expressing cells resulted in PKCdelta cleavage, while inhibition of PKCdelta reduced etoposide-induced apoptosis and prevented Bax activation. Taken together, these findings suggest that Bax and caspase activation, together with PKCdelta signaling are involved in c-Myc-dependent etoposide-induced apoptosis.
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