Synthetic molecule causes cancer cells to self-destruct

From the article:

Most living cells contain a protein called procaspase-3, which, when activated, changes into the executioner enzyme caspase-3 and initiates programmed cell death, called apoptosis. In cancer cells, however, the signaling pathway to procaspase-3 is broken. As a result, cancer cells escape destruction and grow into tumors.

"We have identified a small, synthetic compound that directly activates procaspase-3 and induces apoptosis," said Paul J. Hergenrother, a professor of chemistry at the University of Illinois at Urbana-Champaign and corresponding author of a paper to be posted online this week ahead of regular publication by the journal Nature Chemical Biology. "By bypassing the broken pathway, we can use the cells' own machinery to destroy themselves."

So, the 'trick' is to repair a fault in the cancer cells that stops them from dying off normally. It wouldn't affect other cells, since they already undergo cell death naturally, if I understand correctly.

It sounds like the procaspase-3 is already present in both cancer cells and normal cells, though, and that it is the activation of the protein which causes cell death. I'm assuming that this activation starts the death immediately. It sounds like that found a way to force the activation of the protein, which would make the cell die immediately. My question is how does this affect the normal cells, which also have the same protein?

Maybe I'm wrong and the protein is activated all the time, but has a delayed effect.

It sounds like they plan to use it at the site of the cancer, not as a general treatment. As long as the new compound is used up in the process of activating procaspase-3, it should have minimal effect on surrounding (healthy) tissue.

This is why I'm not a biologist. Waay too complicated. :)

As Adam Kemp said, normal cells also have procaspase 3, and so the very real danger is that it will also get activated. You may be able to control it because cancer cells have more of the procaspase 3. Both kinds of cells have inhibitors of these caspases (IAPs), so I am not sure that there is much there.

Caspases work by a sort of mass action threshold. Once you get enough of them activated, you start a chain reaction, whereby they activate more procaspases and go about chopping the cell up. So you'd have to have very good localization and control over the drug.

In most cancers, there are normal cells mixed in.

I am not hugely optimistic about this rather brute force approach...