The p53 protein is a key factor in the body's natural defence against cancer. Under normal conditions, it initiates death in cells that have begun to divide uncontrollably, mainly by increasing expression of genes that cause cell death. However, research in this month's Nature Cell Biology suggests that p53 performs a more direct role in cell suicide (apoptosis) by interacting with one of the pro-death proteins.
Donna George and colleagues show that some of the cancerous mutations in p53 lie in a region that is important for interactions with the BAK pro-death protein. BAK mediates cell death by piercing holes in mitochondria, resulting in the release of other pro-death proteins that initiate apoptosis. The p53-BAK interaction also prevents BAK from interacting with an anti-death protein that normally prevents BAK from attacking mitochondria. Thus, p53 may induce cell death by interfering with this protective interaction.
Given the prevalence of defective p53 in various cancers, understanding the specific interactions that mediate its function may be the key to future cancer treatments. Drug- or gene-therapy-based treatments that focus on the interaction of p53 with these pro-death proteins should provide exciting alternatives to current cancer therapies.
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(C) Nature Cell Biology press release.
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