RT Journal Article SR Electronic T1 Amentoflavone Inhibits Hepatocellular Carcinoma Progression Through Blockage of ERK/NF-ĸB Activation JF In Vivo JO In Vivo FD International Institute of Anticancer Research SP 1097 OP 1103 DO 10.21873/invivo.11351 VO 32 IS 5 A1 KUN-CHING LEE A1 WEI-TING CHEN A1 YU-CHANG LIU A1 SONG-SHEI LIN A1 FEI-TING HSU YR 2018 UL http://iv.iiarjournals.org/content/32/5/1097.abstract AB Aim: The aim of the present study was to confirm therapeutic efficacy and find probable mechanism of action of amentoflavone in hepatocellular carcinoma (HCC) in vivo. Materials and Methods: Luciferase reporter vector pGL4.50_transfected SK-Hep1 (SK-Hep1/luc2) tumor-bearing mice were treated with vehicle or amentoflavone (100 mg/kg/day by gavage) for 14 days. Tumor growth, amentoflavone toxicity, and extracellular signal-regulated kinase (ERK)/nuclear factor-kappaB (NF-ĸB) signaling in tumor progression were evaluated with digital caliper, bioluminescence imaging, computed tomography, body weight, pathological examination of liver, and immunohistochemistry staining. Results: Amentoflavone significantly inhibited tumor growth, ERK/NF-ĸB activation, and expression of tumor progression-associated proteins as compared to vehicle-treated group. In addition, body weight and liver morphology of mice were not influenced by amentoflavone treatment. Conclusion: These results suggest that amentoflavone inhibits HCC progression through suppression of ERK/NF-ĸB signaling.