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Switching on ‘cancer gene’ could cure heart disease, say scientists

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Switching on 'cancer gene' could cure heart disease, say scientists
An adult mouse heart after activation of both proteins vital for cell replication. (PA)

Switching on a cancer gene could be the key to curing heart disease, Cambridge scientists claim in a scientific breakthrough.

The cancer gene could hold the secrets to the world’s first curative treatment for heart disease.

Cambridge scientists made the discovery while tasked with a separate mission to find out how to turn off a gene that allows cancer to spread.

But they made a surprising U-turn when they realised the gene could actually help heart tissue to repair itself.

By making the cancer gene overactive and functional in the hearts of mice, this triggered heart cell regeneration.

Findings suggest doctors could be able to help the heart to mend itself, even after a heart attack.

Lead study author Dr Catherine Wilson, a researcher at the University of Cambridge, said: ‘This is really exciting because scientists have been trying to make heart cells proliferate for a long time.

‘None of the current heart disease treatments are able to reverse degeneration of the heart tissue, they only slow progression of the disease. Now we’ve found a way to do it in a mouse model.”

Adult mouse heart muscle cells (blue) after activation of both proteins vital for cell replication. Green shows cells replicating. Red marks nuclei of the heart muscle cells. (Dr Cathy Wilson / SWNS)

Heart failure affects around 23 million people worldwide each year, and there is currently no cure. After a heart attack, an adult human heart can lose up to one billion heart muscle cells called cardiomyocytes.

Unlike many other organs in the body, the adult heart cannot regenerate itself, so these cells are never replaced. Their loss reduces the strength of the heart and causes scar formation, heart failure and ultimately death.

The cell cycle, through which cells make copies of themselves, is tightly controlled in mammal cells.

Cancer develops when cells start to replicate themselves uncontrollably, and the Myc gene plays a key role in the process.

Dr Wilson said: ‘Myc is known to be overactive in the vast majority of cancers, so targeting this gene is one of the highest priorities in cancer research.

‘Much recent research has focused on trying to take control of Myc as a means of cancer therapy.’

When researchers made Myc overactive in a mouse model, they saw its cancerous effects in organs including the liver and lungs.

Huge amounts of cells started replicating over the course of a few days but in the heart, nothing happened.

They found that Myc-driven activity in heart muscle cells is critically dependent on the level of another protein called Cyclin T1, made by another gene called Ccnt1 within the cells.

When the Ccnt1 and Myc genes are expressed together, the heart switches into a regenerative state and its cells start to replicate.

Dr Wilson said: ‘When these two genes were overexpressed together in the heart muscle cells of adult mice, we saw extensive cell replication leading to a large increase in the number of heart muscle cells.’

Using next generation technology, the researchers were able to observe the behaviours of the Myc gene in the heart cells.

Myc produces a protein which binds to the DNA in specific cells and activates gene expression, which helps to create proteins.

Muscle cells (blue) after activation of both proteins vital for cell replication. Red shows cells replicating. Green marks cell membrane. (Dr Cathy Wilson / SWNS)

But despite the protein binding successfully, the heart cells did not start to replicate themselves because the protein could not activate gene expression,

Another protein vital to gene expression, Cyclin T1, was deficient in the heart. Adding it to the cells with the overactive Myc caused the cells to start rapidly multiplying.

Dr Wilson said: ‘None of the current treatment options can reverse the degeneration of heart tissue.

‘The inability of the heart to regenerate itself is a significant unmet clinical need.

‘We found that even when Myc is switched on in a heart, the other tools aren’t there to make it work, which may be one of the reasons heart cancer is so extremely rare.

‘Now we know what’s missing, we can add it and make the cells replicate.’

As the world’s population grows and the prevalence of heart failure increases, the cost of patient care is anticipated to increase dramatically.

The researchers hope to develop their research into a genetic therapy for the treatment of heart disease.

Dr Wilson added: ‘We want to use short-term, switchable technologies to turn on Myc and Cyclin T1 in the heart.

‘That way we won’t leave any genetic footprint that might inadvertently lead to cancer formation.’

The study was published in the journal Nature Communications.

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