“Molecular Switch” Helps Breast Cancer Spread: Scientists Identify a Way to Turn It Off

Australian scientists have identified a molecular mechanism that may play a key role in the spread of triple-negative breast cancer, one of the most aggressive forms of the disease. The researchers also found that an existing cancer drug can suppress the growth of metastases in laboratory models. The study was published in EMBO Molecular Medicine.

Triple-negative breast cancer is particularly difficult to treat because its cells lack receptors for estrogen and progesterone as well as the HER2 protein, which are targets of many modern therapies. Despite advances in immunotherapy, treatment options remain limited when the disease returns.

Researchers from the University of Adelaide and the Olivia Newton-John Cancer Research Institute identified an important role for a molecule called miR-342. It regulates a network of genes involved in tumor development. When levels of miR-342 fall, activity in the E2F signaling pathway increases. According to the scientists, this may allow tumor cells that have already spread through the body to begin forming new metastatic sites.

The analysis showed that patients with low levels of miR-342 and high E2F activity were more likely to develop metastatic disease.

The researchers then restored miR-342 levels in preclinical models. This significantly reduced the spread of tumors to other organs, including the lungs and bones.

Another finding was particularly promising. Palbociclib, a CDK4/6 inhibitor already used to treat advanced hormone receptor-positive breast cancer, substantially suppressed the growth of metastatic tumors in models with low miR-342 levels. The strongest effect was observed when the drug was administered after tumor cells had already spread.

According to the researchers, measuring miR-342 levels could eventually help identify patients with triple-negative breast cancer who might potentially benefit from CDK4/6 inhibitors.

The next step will be to test the findings in models developed from individual patients' tumors, after which the researchers hope to move toward clinical trials. The authors stress, however, that this is still a promising potential treatment strategy rather than a proven therapy.