AKT1 and neoplasm: Since vasohibin-1 overexpression did not inhibit cellular invasion, we continued screening of the mediator proteins, and found that IGF-1 expression was inhibited by migracin A. IGF-1 is known to drive tumor cell motility as an upstream effector of the PI3K/Akt signaling pathway, in that it activates cell proliferation, survival, migration and angiogenesis in several cancer cells [21].