Now we are really getting there, Kenyon said.
The gene daf-2 codes for a receptor for insulin and also for an insulin-like protein that promotes growth. It influences daf-16, which makes a so-called transcription factor a protein that determines when and where hundreds of other genes are turned on. The focus of the new study was to identify specific genes regulated by daf-16 which affect cancer and/or lifespan.
The scientists used an established tumor model in the worms. Then, starting with a list of 734 genes known to be targets of daf-16, they identified 29 genes that either promote or suppress tumor cell growth. They did this using several techniques, including RNA interference or RNAi, a powerful tool that allows scientists to control the expression of just one kind of gene at a time.
About half of the genes stimulated tumor growth and half suppressed it, they found. Strikingly, about half of these genes also affect lifespan in animals that do not have tumors, further strengthening the model Kenyon and others have conceived in which the insulin receptor, daf-2, works in concert with the transcription factor daf-16 to link longevity and tumor resistance. The downstream genes appear to act in a cumulative way, they found.
The genes that stimulated tumor growth also accelerated aging itself, and the genes that prevented tumor growth slowed down the aging process and extended lifespan. These findings greatly strengthen the view that the controls of lifespan and cancer have deep, common roots, Kenyon and Pinkston conclude.
|Contact: Wallace Ravven|
University of California - San Francisco