IGF1 and cancer: In cancers, however, under hypoxia or stimulation from IGF-1, HIF-1α is stabilized due to the inhibition of prolyl hydroxylase and translocates into the nucleus, where it dimerizes with constitutively expressed HIF-1β, and this HIF-1α/β dimer can bind to hypoxia-response elements of angiogenic growth factors (Figure 2) [71].