✦ LIBER ✦

2-methoxyestradiol induces caspase-independent, mitochondria-centered apoptosis in DS-sarcoma cells

✍ Scribed by Christine Lambert; Katrin Apel; Hans Konrad Biesalski; Juergen Frank

Publisher: John Wiley and Sons
Year: 2003
Tongue: French
Weight: 315 KB
Volume: 108
Category: Article
ISSN: 0020-7136
DOI: 10.1002/ijc.11579

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✦ Synopsis

Abstract

The anti‐cancer potential of the natural estrogen metabolite 2‐methoxyestradiol is associated with microtubuli interaction, anti‐angiogenetic effects and inhibition of superoxide dismutase leading to apoptosis. The effectors of apoptotic signaling through 2‐methoxyestradiol, however, are cell type‐dependent. We investigated the effect of 2‐methoxyestradiol on several events associated with apoptosis in rat DS‐sarcoma cells. Translocation of the pro‐apoptotic protein Bax to mitochondria was identified as an initial apoptotic event that was accompanied by a decrease in mitochondrial transmembrane potential and the formation of reactive oxygen species (ROS) followed by mitochondrial release of apoptosis inducing factor and endonuclease G. In addition, 2‐methoxyestradiol treatment caused upregulation of death receptor ligands FasL and TNFα and induced caspase‐8 activation. The pan caspase inhibitor Z‐VAD‐FMK did not suppress apoptotic cell death, however, indicating that the major pro‐apoptotic effect of 2‐methoxyestradiol is mediated by a caspase‐independent mechanism. Furthermore, ROS do not seem to play a pivotal role in the toxic/apoptotic effect of 2‐methoxyestradiol in DS‐sarcoma cells because supplementation with various antioxidants provided only limit protection. Colony formation was not affected by antioxidants. Therefore, in DS‐sarcoma cells, the breakdown of mitochondrial integrity with the subsequent release of mitochondrial nucleases is the main factor in 2‐methoxyestradiol mediated cell death. © 2003 Wiley‐Liss, Inc.

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