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. 2014 Jul 8;5(15):6142–6167. doi: 10.18632/oncotarget.2178

Fig.7. Inhibition of AKT modulates p53 stability in-vivo and synergizes with ionizing radiation to inhibit tumor growth.

Fig.7

(A) PSN1 xenografts (PSN1 cells co-injected with LTC-14 stellate cells) established in the flank of athymic nude mice were treated with MK-2206 (60 mg/kg-320 mg/kg) as indicated or β-cyclo-dextrin (1.5 mg/ml) carrier. Xenograft tumors were lysed and lysates probed by western blot with the indicated antibodies. (B-D) Sections of PSN1 xenografts treated with three consecutive doses of MK-2206 (60 mg/kg). (B) Sections of PSN1 xenografts and in-vitro PSN1 cells fixed and stained with anti-NPM (red) and anti-p14ARF (green). (C) PSN1 xenografts treated with MK-2206 or carrier were stained with DAPI, anti-p53 (DO1) or p53mut (OP29 clone) (D) PSN1 xenografts treated with MK-2206 (60 mg/kg) or carrier were stained by immunohistochemical methods with anti-pS473-AKT, anti-phospho-S48-NPM (pS48-NPM) or p53. (E) PSN1 xenografts established in the flank of athymic nude mice were injected subcutaneously with two alternate day doses of MK-2206 (60 mg/kg) or carrier. Mice were subsequently treated with a single dose of IR (6 Gy) and tumor volumes measured regularly with callipers. Dash lines indicate tumor growth differential at 250 mm3.