Beta Blockers May Halt Progression of Aggressive Breast Cancer, Study Finds
A recent study has discovered a molecular biomarker that could identify triple negative breast cancer (TNBC) patients who may benefit from beta blocker therapy to prevent tumour progression.
Researchers at Monash University found that the interplay between two cell signals, cAMP and calcium, can trigger cancer progression when the β2-adrenoceptor is active.
A gene called HOXC12 is central to switching this interplay on and off.
By deleting HOXC12 using the CRISPR-Cas9 gene-editing tool, the team stopped the β2-adrenoceptor-cAMP-calcium interplay, indicating that HOXC12 could be the key to identifying patients who will respond to beta blocker therapy.
Background
TNBC is an aggressive cancer that can be challenging to treat.
Beta blockers, a class of medication used to block the effects of stress hormones, have been identified as a potential therapeutic option for halting cancer progression in TNBC patients.
Previous studies have shown that beta blockers are associated with a significant reduction in mortality in people with TNBC, but the reason behind this correlation was unknown.
The latest study, published in Science Signaling, suggests that HOXC12 is a key mediator of the β2-adrenoceptor-cAMP-calcium ‘feedforward loop’ in TNBC.
Analysis of a comprehensive patient genomic database showed that high levels of HOXC12 expression in TNBC patients were associated with poorer overall survival.
Implications
The discovery could pave the way for improving survival outcomes in people with TNBC when HOXC12 is found to be present.
According to Associate Professor Michelle Halls, senior author of the study, “If HOXC12 is present in a TNBC patient, they could be an ideal candidate for beta blocker therapy.”
Further studies are needed to determine if HOXC12 can be used to identify patients who will benefit from beta blocker therapy at the time of diagnosis and stop tumour spread, thus increasing survival rates.