Mice studies have revealed that loss of one of sirtuin (SIRT1) enzyme drives the formation of early prostate cancer (prostatic intraepithelial neoplasia, PIN).
SIRT1 can defend the cell against damage from free radicals. Researchers created a mouse model that lacked SIRT1. Normally SIRT1 proteins help activate a mitochondrial protein called SOD2, in turn activating those proteins to keep free-radical levels in check. When SIRT1 levels diminish, SOD2 is no longer effective at removing free radicals, allowing a dangerous build up in the cells, and leading to PIN.
Lead researcher Dr. Richard Pestell said, "Using genetic deletion we found that SIRT1 normally restrains prostatic intraepithelial neoplasia in animals. Therefore too little SIRT1 may be involved in the cellular processes that starts human prostate cancer. As we had shown that gene therapy based re expression of SIRT1 can block human prostate cancer tumor growth, and SIRT1 is an enzyme which can be targeted, this may be an important new target for prostate cancer prevention."
The research is published online in 'The American Journal of Pathology'.