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Perspectives

Does Caspase Inhibition Promote Clonogenic Tumor Growth?

Ute Fischer, Katja Janssen and Klaus Schulze-Osthoff

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Defects in the control of cell death are a major cause of resistance to tumor therapy. Until recently, components of the intrinsic apoptotic pathway that act downstream of mitochondria, such as the caspases, have been apportioned only a minor share in this business. Thus, defects in mitochondrial caspase activation were suggested to cause apoptosis inhibition but not to confer clonogenic survival. This assumption was based on the finding that chemotherapeutic agents provoke mitochondrial damage even the absence of caspases, resulting in the release various toxic mediators and a subsequent caspase-independent cell death. In contrast to these earlier observations, we recently showed that in the absence of active caspases tumor cells do not necessarily undergo caspase-independent cell death but may even survive a chemotherapeutic insult. Our findings suggest that caspase inhibition can indeed promote clonogenic tumor growth which might be not only relevant for tumor therapy but should be also considered when evaluating the safety of therapeutic caspases inhibitors.

Authors

Ute Fischer

Heinrich-Heine-University Düsseldorf; Düsseldorf, Germany

Katja Janssen

Heinrich-Heine-University Düsseldorf; Düsseldorf, Germany

Klaus Schulze-Osthoff

Heinrich-Heine-University Düsseldorf; Düsseldorf, Germany

Purchase article for $19

Subscribe to this journal for $129/year