According to researchers at the University of California, San Francisco, their study underscores the deep evolutionary connection between lifespan and cancer. They also said their findings indicate that cellular changes leading to longevity antagonize tumour cell growth.
The scientists found that many of the worm genes have counterparts in humans, suggesting that new drugs may some day ensure a long, cancer-free life.
Study author, Cynthia Kenyon previously carried out a study in worms in 1993, wherein she found that a change in just one gene, called daf-2, doubled the worms' lifespan.
This finding led to the understanding that lifespan is regulated by genes and is therefore changeable, rather than the inevitable result of the body's breakdown. The discovery in worms has been confirmed in other animals including mice.
"There is a widely held view that any mechanism that slows aging would probably stimulate tumour growth. But we found many genes that increase lifespan, but slow tumour growth. Humans have versions of many of these genes, so this work may lead to treatments that keep us youthful and cancer-free much longer than normal," Nature quoted Kenyon, as saying.
Since her early finding that the gene daf-2 and another gene known as daf-16 regulate lifespan, her research team has hoped to identify the genes that they in turn affect -- those that more directly affect aging and tumour growth.
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.
For the study, the scientists used an established tumour 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 tumour 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.
The results showed that about half of the genes stimulated tumour growth and half suppressed it. Strikingly, about half of these genes also affect lifespan in animals that do not have tumours, 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 tumour resistance.
The genes that stimulated tumour growth also accelerated aging itself, and the genes that prevented tumour growth slowed down the aging process and extended lifespan.
Kenyon concluded that these findings greatly strengthen the view that the controls of lifespan and cancer have deep, common roots.
The new research is published in the journal "Nature Genetics."