VDAC1 and breast cancer: 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).