The discovery could also pave the way for improved early diagnostics.
Peter Storz and colleagues tested the drug, decitabine, in a mouse model of breast cancer where it shrank the primary breast tumour and minimised metastasis to the animals' lungs. Mice treated with drug had very few or no metastases in their lungs, and those that were found were around 40 times smaller than those observed in untreated control animals. Decitabine, or drugs that work in a similar way, could be used to help manage breast cancer, the authors say, but human studies will be needed.
The drug works by targeting a particular gene, called PRKD1. Normally, the gene is switched on, but in invasive breast cancer, gene-inactivating molecules called methyl groups bind to the DNA next to the gene, switching it off. Decitabine prevents these methyl groups from binding to DNA.
Treatment with the drug reduced methylation levels around the PRKD1 gene. As a result, the gene was switched back on, and was able to start churning out protein as normal.
The authors also studied methylation levels in human breast cancer tissues with varying degrees of invasiveness. Methylation levels correlated with the cancer's potential to spread. The finding could, the authors say, be used to help generate a new diagnostic test that could predict how likely breast cancer is to metastasize.
Decitabine is one of a handful of FDA-approved cancer drugs that work via epigenetics, influencing the structure and form of DNA to affect gene expression, without altering the DNA sequence itself. Alongside genetic changes, epigenetic differences are now known to play a role in many different types of tumour, including prostate and cervical cancer. Decitabine is currently licensed for the treatment of acute myeloid leukaemia, a cancer of white blood cells.