LONDON (Reuters) - One of the genes that protects us from cancer may also help delay ageing, according to a new study published on Wednesday.
The findings could also one day lead to new drugs that prevent or fight cancer while extending healthy youth and lifespan, said Manuel Serrano, a researcher at the Spanish National Cancer Research Centre, who worked on the study.
Serrano said researchers genetically engineered mice to have an extra copy of a key cancer-fighting gene called p53 and found it also played an important role in delaying ageing.
“Everyone agrees that the ageing is produced by the accumulation of faulty cells,” Serrano said. “In other words, p53 delays ageing for exactly the same reason that it prevents cancer.” The study was published in the journal Nature.
Previous cancer studies have shown that p53 can actually cause premature ageing symptoms by killing too many cells when it goes into overdrive, but Serrano said his research strictly regulated the gene so that it turned on only when needed.
The gene -- and another that regulates signals to p53 -- did their normal job of producing a protein that kills damaged cancer cells. But the researchers found that mice with an extra copy of the genes actually lived longer even when stripping out the impact of having less cancer.
“This is the first anti-cancer gene tested for its effect on ageing,” Serrano said. “The mice lived 16 percent longer in their average lifespan.”
The p53 gene, when working properly, makes sure that damaged cells destroy themselves and do not divide uncontrollably to cause tumors. If the gene is mutated or inactivated the control mechanism does not work.
The role of p53 in cancer has been known for many years and Serrano said he and his team simply applied this knowledge to the problem of ageing and targeting damaged cells.
“The expectation is that having more p53, mice will have a stricter quality control for cells, hence less cancer and less ageing,” he said in a telephone interview.
Serrano also said that other research has shown that mice and worms that eat less have slower metabolisms and live longer. But his study offers evidence that the mice can benefit from the extra copy of the genes without having to be starved.
While the study opens up possibilities for drugs based on p53 that delay ageing, researchers will need to find the right balance in boosting the gene to prevent potentially harmful effects, he said.
“There are a number of chemical compounds that have been developed by the big pharmaceutical companies and these compounds are able to boost p53 in the organism,” he said.
“These compounds are being tested now for their possible anti-cancer activity and hopefully in the light of our study also for their possible anti-ageing activity.”