These authors contributed equally to this work.
Novel anti-apoptotic effect of Bcl-2: Prevention of polyamine depletion-induced cell death
Article first published online: 2 JAN 2013
© The Author(s) Journal compilation © 2008 International Federation for Cell Biology
Cell Biology International
Volume 32, Issue 1, pages 66–74, January 2008
How to Cite
Holst, C. M., Johansson, V. M., Alm, K. and Oredsson, S. M. (2008), Novel anti-apoptotic effect of Bcl-2: Prevention of polyamine depletion-induced cell death. Cell Biology International, 32: 66–74. doi: 10.1016/j.cellbi.2007.08.011
- Issue published online: 2 JAN 2013
- Article first published online: 2 JAN 2013
- Received 13 February 2007; revised 29 June 2007; accepted 22 August 2007
- Spermine analogue;
- Cytochrome c;
- Human breast cancer
The spermine analogue N1,N11-diethylnorspermine (DENSPM) efficiently depletes the polyamine pools in the breast cancer cell line L56Br-C1 and induces apoptotic cell death via the mitochondrial pathway. In this study, we have over-expressed the anti-apoptotic protein Bcl-2 in L56Br-C1 cells and investigated the effect of DENSPM treatment. DENSPM-induced cell death was significantly reduced in Bcl-2 over-expressing cells. Bcl-2 over-expression reduced DENSPM-induced release of the pro-apoptotic proteins AIF, cytochrome c, and Smac/DIABLO from the mitochondria. Bcl-2 over-expression reduced the DENSPM-induced activation of caspase-3. Bcl-2 over-expression also prevented DENSPM-induced Bax cleavage and reduction of Bcl-XL and survivin levels. The DENSPM-induced activation of the polyamine catabolic enzyme spermidine/spermine N1-acetyltransferase was reduced by Bcl-2 over-expression, partly preventing polyamine depletion. Thus, Bcl-2 over-expression prevented a number of DENSPM-induced apoptotic effects.