Beta blockers could halt triple-negative breast cancer, new study suggests

Wednesday, 20 August 2025 08:04

Australian researchers have uncovered a potential way to stop the spread of triple negative breast cancer, an aggressive and often difficult-to-treat form of the disease.

Australian researchers have uncovered a potential way to stop the spread of triple-negative breast cancer (TNBC), an aggressive and often difficult-to-treat form of the disease.

A new study by Monash University researchers has identified a key genetic switch that could determine which triple-negative breast cancer patients could benefit from beta blocker therapy.

The findings, published in the journal Science Signaling, identify a specific gene that acts as a "switch" for tumour progression, and could help doctors determine which patients would benefit from beta blocker medication.

A woman receives radiation therapy treatment for breast cancer.

Beta blockers are a class of drugs commonly used to treat high blood pressure and other heart conditions.

They work by blocking the blocking stress hormones.

However, Monash researchers have been investigating their potential to fight cancer.

Previous studies by the university have shown a link between beta blocker use and improved outcomes for some TNBC patients, but the reason for this was unclear - until now.

The science behind the switch

The Monash Institute of Pharmaceutical Sciences team focused on the body's natural stress response.

When stress hormones are released, they can activate a receptor called the "beta-2 adrenoceptor," which can accelerate the spread of cancer cells.

The researchers discovered that a complex interplay between two cellular signals, cAMP and calcium, is triggered by the beta-2 adrenoceptor, fuelling cancer progression.

At the centre of this process is a single gene, HOXC12, which acts as the master regulator.

Using the gene-editing tool CRISPR-Cas9, the scientists were able to "delete" the HOXC12 gene, which effectively "switched off" the cancer-promoting cellular signals.

This suggests that the presence of the HOXC12 gene could be the key to identifying patients who would respond well to beta blocker therapy, which works by blocking the effects of stress hormones.

New hope for patients

Associate Professor Michelle Halls, a senior author of the study from MIPS, said the discovery was exciting.

"Our colleagues at MIPS, who were also pivotal to this latest study, have previously found that beta blockers are associated with a significant reduction in mortality in people with TNBC," she said.

"Now we have a much better grasp on why this could be the case. In the Science Signaling study we looked at several TNBC cancer cell types and found that one gene in particular, HOXC12, is a key mediator of the β2-adrenoceptor-cAMP-calcium 'feedforward loop' in TNBC.

"This information means that if HOXC12 is found to be present in a TNBC patient, they could be an ideal candidate for beta blocker therapy."