How Might This Cheap Painkiller Be Able To Stop Some Cancers From Spreading?

How Might This Cheap Painkiller Be Able To Stop Some Cancers From Spreading?



A team of researchers from the University of Cambridge believe they have uncovered the mechanism behind how aspirin, a common and inexpensive painkiller, might be able to stop cancer from spreading – and they made this discovery somewhat by accident.

What they’d been looking at was how the immune system responds to metastasis. This is when single cancer cells break away from the initial tumor and spread elsewhere in the body, and it’s the primary cause of death for more than 90 percent of people with cancer.

However, the loneliness of these rogue cells also makes them a prime target for T-cells. These are the front-line soldiers of the immune system, designed to attack and destroy infected and cancerous cells, which is much easier when those cells are on their own.

When the team was screening mice for immune system-related genes that might be involved in metastasis, they came across something interesting that involved T-cells – a gene that was suppressing their activity, known as Arhgef1. When they studied mice that didn’t have Arhgef1 in their T-cells, those mice experienced less metastasis from the original tumor to the lungs and liver.

But Arhgef1 wasn’t the root cause of the T-cell problem – there was something else controlling it, and that’s where the team uncovered a surprising link to aspirin.

The researchers discovered that the T-cell suppressing gene was being switched on by a protein produced by platelets, fragments of cells that help blood to clot. However, clotting can sometimes be a problem; aspirin reduces the amount of the clotting protein, called thromboxane A2 (TXA2), produced.

Previous research had suggested that taking a low dose of aspirin on a daily basis could also help to prevent metastasis – what this team had just figured out was how.

“It was a Eureka moment when we found TXA2 was the molecular signal that activates this suppressive effect on T cells. Before this, we had not been aware of the implication of our findings in understanding the anti-metastatic activity of aspirin. It was an entirely unexpected finding which sent us down quite a different path of enquiry than we had anticipated,” first author Dr Jie Yang said in a statement.

The team’s findings were tested on two groups of mice with a type of cancer called melanoma: one group was given aspirin, while the other was not (known as a control group). The results showed that, compared to the control group, metastasis was less frequent in the mice that were given aspirin, and that this involved T-cells.

This doesn’t mean that everyone with cancer should run to the drugstore and stock up on aspirin. Not only is further research needed – carried out in humans, seeing as we’re not quite the same as mice – but regular aspirin use can also have side effects, including stomach ulcers and bleeding more easily.

Still, the results are promising. If aspirin proves to be a viable treatment, its low cost would make it an attractive one, too.

“Aspirin, or other drugs that could target this pathway, have the potential to be less expensive than antibody-based therapies, and therefore more accessible globally,” Yang added.

The study is published in Nature.



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