To further investigate the interactions of uPAR with several tumour-promoting proteins, uPA was confirmed and IGF1R was identified as direct interactor in the TNBC cohort and these complexes significantly correlated with cathepsin B and D, whereas IGF1R significantly correlated with cathepsin B and not with cathepsin D. Previous studies have shown cathepsins being correlated with uPAR or uPA and involved in metastasizing processes of breast cancer cells [15, 49] emphasizing the malignant potential of these interactions in TNBC. This evidence concerns the gene IGF1R and breast cancer.