Conversely, prolonged FR58P1a treatment generates a metabolic adaptation toward glycolysis that includes an upregulation of the glucose transporter 4 (GLUT4), which is known to play an essential role in basal glucose uptake in breast cancer cells promoting proliferation and survival under hypoxic conditions78, a downregulation of OXPHOS-related genes (cox-iv isoform 1, cyt c, atp5fa1), reduced cardiolipin content, and reduced expression of respiratory complexes (II, IV, V) and proteins of outer mitochondrial membrane (VDAC, TOMM20). Here, VDAC1 is linked to breast carcinoma.