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Susceptibility to drug-induced apoptosis correlates with differential modulation of Bad, Bcl-2 and Bcl-x(L) protein levels

  1. Author:
    Tudor, G.
    Aguilera, A.
    Halverson, D. O.
    Laing, N. D.
    Sausville, E. A.

  2. Author Address

    Tudor G NCI, Frederick Canc Res & Dev Ctr, Sci Applicat Int Corp POB B Frederick, MD 21702 USA NCI, Frederick Canc Res & Dev Ctr, Sci Applicat Int Corp Frederick, MD 21702 USA NCI, Div Canc Treatment, Dev Therapeut Program Rockville, MD 20892 USA
    1. Year: 2000
  2. Journal: Cell Death and Differentiation
    1. 7
    2. 6
    3. Pages: 574-586
  4. Type of Article: Article
  1. Abstract:

    To define the responses of apoptotic regulatory proteins to different chemotherapeutic agents, we investigated the expression of Bcl-2 family gene products, the release of cytochrome c, and the activation of pro-caspase-3 during apoptosis induced by Taxol and Thiotepa, in the MCF-7 breast carcinoma and the HL-60 leukemia cell lines. The earliest event induced by drug exposure was increase in Bad protein levels, followed by Bcl-2 down-regulation, cytochrome c release, and Bcl-x(L) and Bar up-regulation. Bak accumulation was a late event. Activation of pro-caspase-3 and cleavage of Bcl-2 protein occurred in the HL-60 cells only, and followed the cytochrome c release. The overall responses were qualitatively similar in both cell types, but MCF-7 cells treated with Taxol showed a significant delay in apoptosis, correlating with early up-regulation of Bcl-2 and delayed release of cytochrome c, We conclude that Bad up-regulation is an early indicator of a cellular response that will lead to cell death, but may be modulated by survival mechanisms, which cumulatively govern the ultimate susceptibility to apoptosis. [References: 59]

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