AST inhibits tumor growth and suppresses tissue VEGF level by modulating Akt/mTOR signaling and COX-2. HCT 116 colon cancer cells (2 × 106) were injected subcutaneously to the Balb/c nu/nu mice. AST (100 mg/kg) was administrated orally once daily for 14 days after the tumors became palpable at Day 10. Tumors from the xenografted mice were excised at the day of sacrifice. (A) Tumor volume and (B) serum VEGF level in the control and AST-treated groups of animals were measured. Data are expressed as mean ± S.E.M. (n = 6), with statistical significance * p < 0.05, ** p < 0.01 when compared with control group. (C) Tissue level of p-Akt, Akt, p-mTOR, mTOR, and (D) the pro-angiogenic factors VEGF, VEGFR1 and VEGFR2 was examined in untreated control (#1-2) and AST-treated (#3-4) groups of animals. Representative immunoblots from tumor tissues obtained from six animals in each group are shown. β-actin was used as internal control in immunoblot assay. (E) Histological examination of COX-2 level in tissue sections of HCT 116 xenografted nude mice with or without AST treatment was performed. Representative microphotographs of control and drug-treated groups are shown (200x magnification).