The team form Metastasis Research Laboratory (GIGA Cancer, ULg) has recently demonstrated that myoferlin regulates epidermal growth factor signaling in breast cancer by affecting intracellular handling of the activated epidermal growth factor receptor. Motivated by these results, the ULg researchers in collaboration with the Department of Molecular Pharmacology and Oncology (Gunma University Graduate School of Medicine, Japan) have investigated myoferlin expression in triple-negative breast cancer cells (TNBC). Their data show that myoferlin is overexpressed in the majority of TNBC cells, both at mRNA and protein level.

Intrigued by these findings the investigators assessed proteomics, metabolomics and ultrastructural changes following myoferlin suppression. They found that myoferlin is an essential component of the cellular endosomal machinery, regulating fatty acid household, mitochondrial function and, hence, global metabolism in TNBC cells.

High levels of myoferlin conferred metabolic flexibility to TNBC cells, allowing them to adapt to hostile environments and, hence, increase their metastatic potential. The significance of this observation was further supported by clinical data, showing that TNBC patients, whose tumors overexpress myoferlin, have worst distant metastasis-free and overall survivals. This novel insight into myoferlin function establishes an important link between vesicle traffic, cancer metabolism and progression, offering new diagnostic and therapeutic concepts to develop treatments for TNBC patients.