No specific treatments are currently available for triple negative breast cancer (TNBC), a type of tumour that lacks the receptors targeted by many breast cancer therapies.

Although many TNBC tumours lack two tumour suppressors, RB1 and p53, the specific downstream pathways that can be targeted as potential treatments for these tumours have not been identified.

In this issue of the JCI, a team led by Eldad Zacksenhaus at Toronto General Research Institute discovered that the growth of TNBC-like breast tumours is supported by enhanced mitochondrial function.

Mice carrying tumours that were deficient in both RB1 and p53 displayed upregulation of a pathway that controls the synthesis of mitochondrial proteins.

They then identified an FDA-approved drug, tigecycline, that blocks this upregulation and reduces the growth of TNBC-like tumours in mice.

This work suggests that inhibiting mitochondrial protein translation could potentially be a successful treatment for TNBC.

Source: JCI