HIF1A and glioblastoma: Evidence suggests that the mechanism underlying HIF-1α melatonin-dependent regulation might be cell type specific; hence, in U251 and U87 glioblastoma cells [47], and in HCT116 colon cancer cells [23], melatonin prevents ROS-dependent PHDs inactivation, promoting HIF-1α proteasomal degradation under hypoxia [25].