Resumen
Here, we demonstrate that the hypoxia-induced cleaved form of VDAC1 (VDAC1-?C) reprograms the cell to utilize more metabolites and is implicated in up-regulation of glycolysis and mitochondrial respiration, conferring a direct survival advantage in hypoxic microenvironment. We further highlight a direct relationship between VDAC1-?C, the primary cilium and cell metabolism.