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. 2008 Aug 26;3(8):e3065. doi: 10.1371/journal.pone.0003065

Figure 4. AKTi-1/2 effectively suppresses HER2-overexpressing and PIK3CA-mutated tumor growth in vivo.

Figure 4

(A) AKTi-1/2 inhibits Akt followed by dephosphorylation of its downstream targets (GSK3, Foxo, p70S6K, S6 and 4EBP1), loss of D-cyclin expression, Rb hypophosphrylation and induction of PARP cleavage in BT474 xenograft tumors. Mice with established BT474 xenografts were treated with AKTi-1/2 100 mg/kg for the indicated times. Tumor lysates were immunoblotted with the indicated antibodies. (B) Mice with established BT474 xenografts were treated with AKTi-1/2 50 and 100 mg/kg/day×5 days/week or vehicle only as control. The results represent the mean tumor volume±standard error (n = 5 mice per group) from two independent experiments. *, P<0.005, 50 versus 100 mg/kg AKTi-1/2, and 50 and 100 mg/kg AKTi-1/2 versus control. (C) Representative immunohistochemistry fields of BT474 tumors from mice euthanized 6 h after the final treatment of AKTi-1/2 as in (B). Tumors were excised, and H&E, phosphorylated Akt, Ki67 and TUNEL were assessed by immunohistochemic statining. (D) Mice with established MCF7 xenografts were treated with AKTi-1/2 50 and 100 mg/kg/day×5 days/week or vehicle only as control. The results represent the mean tumor volume±standard error (n = 5 mice per group) from two independent experiments. *, P<0.005, 50 versus 100 mg/kg AKTi-1/2, and 50 and 100 mg/kg AKTi-1/2 versus control.