Worm links cancer risk to ageing

Scientists have discovered that a naturally produced protein that helps protect us from cancer may also determine how long we live.

The findings – published in the highly respected journal Science – open up a new avenue of inquiry into ageing as a risk factor for cancer.

"We have discovered that proteins that prevent cancer in humans by ensuring that cells don't divide if they are damaged also determine lifespan in the nematode worm," explained Professor Gordon Lithgow, who carried out the work at The University of Manchester.

"Our research has shown that these 'checkpoint proteins' – thought only to operate in cells that divide – function in cells that no longer divide as well. The fact that they appear to have dual functions opens a new way to study the connection between ageing and cancer."

Scientists have long known that, statistically, ageing is a huge factor for cancer but have so far struggled to understand why that is.

Professor Lithgow said: "If we look at checkpoint proteins as a gear, we have known for a long time that they drive the cancer engine; now we know that they also drive the longevity engine. This discovery has exciting potential as an area of inquiry into potential cellular links between ageing and cancer."

The research, which was completed at the Buck Institute in California where Dr Lithgow now works, involved genetically removing checkpoint proteins in the microscopic worm C. elegans. By doing so, the researchers caused a 15-30% increase in the worm's lifespan.

"Given the role that checkpoint proteins play in the development of cancer – or in causing tumours when the proteins are defective – the findings raise the question of whether genetic variations in these proteins in humans places some individuals at risk of cancer.

"Conversely, the checkpoint proteins may set a genetic course for a shorter life but one that is free from cancer."

Dr Dale Bredesen, Chief Executive and Scientific Director at the Buck Institute, added: "This work brings a new richness and sophistication to the way we think about longevity interventions.

"If we're smart about it, we might be able to design strategies where you could keep checkpoint proteins active in dividing cells and stop them working in cells that no longer divide, such as brain cells.

"Increasing the survival of brain cells or 'neurons' could provide a new avenue of treatment for neurodegenerative diseases like Alzheimer's."

Source: University of Manchester
 

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