http://insciences.org/article.php?article_id=8502

A research team led by the University of Colorado at Boulder has discovered a previously unknown cellular "switch" that may provide researchers with a new means of triggering programmed cell death, findings with implications for treating cancer.

The new results are a big step forward in understanding programmed cell death, or apoptosis, a cell suicide process that involves a series of biochemical events leading to changes like cell body shrinkage, mitochondria destruction and chromosome fragmentation, said CU-Boulder Professor Ding Xue. But unlike traumatic cell death from injury, programmed cell death is a naturally occurring aspect of animal development that may help prevent human diseases like cancer and autoimmune disorders, said Xue, lead author on the new study.

In the new study, Xue and his team found that a well-known cellular molecule called caspase – known as the "executioner enzyme" for apoptosis because of its primary role of cutting up and destroying cellular proteins -- has an entirely different effect on a particular enzyme called Dicer. The team found that when caspase cleaves Dicer, it does not kill it but instead changes its function, causing Dicer to break up chromosomes -- pieces of coiled DNA containing thousands of genes -- and kill the cells that house them.

"This finding was totally unexpected," said Xue of CU-Boulder's molecular, cellular and developmental biology department. "We believe that by understanding this mechanism, we may be able to develop a new way to trigger cell death in a controlled manner as a way to treat disease."