PT  - JOURNAL ARTICLE
AU  - LEE, KUN-CHING
AU  - CHEN, WEI-TING
AU  - LIU, YU-CHANG
AU  - LIN, SONG-SHEI
AU  - HSU, FEI-TING
TI  - Amentoflavone Inhibits Hepatocellular Carcinoma Progression Through Blockage of ERK/NF-ĸB Activation
AID  - 10.21873/invivo.11351
DP  - 2018 Sep 01
TA  - In Vivo
PG  - 1097--1103
VI  - 32
IP  - 5
4099  - http://iv.iiarjournals.org/content/32/5/1097.short
4100  - http://iv.iiarjournals.org/content/32/5/1097.full
SO  - In Vivo2018 Sep 01; 32
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.