Caspase-3 normally exists as a proenzyme, meaning further processing is required to make the final, active enzyme, the researchers said. That processing is normally performed by other caspases and serves as a signal that something has gone wrong with a cell and cell death or 'apoptosis' is desired.

Paul Hergenrother and colleagues at the University of Illinois-Urbana say they've used the synthetic compound PAC-1 to trick procaspase-3 into processing itself, generating caspase-3 and causing cell death. They demonstrated, in a variety of cancer cell types, that cell death is correlated with the amount of procaspase-3 present in the cells, with more procaspase-3 resulting in cell death at lower concentrations of PAC-1, while healthy cells remain unaffected.

The researchers say the variability of procaspase-3 levels in the cell lines means some patients would be more responsive to such therapy than others. As such, they say their finding potentially offers a novel opportunity for individualized cancer therapy.

The study appears in the journal Nature Chemical Biology.

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