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) tumorbearing 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-κB) 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-κB 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-κB signaling.
- Bioluminescence imaging
- Extracellular signal-regulated kinase
- Hepatocellular carcinoma
- Nuclear factor-kappaB
ASJC Scopus subject areas
- Biochemistry, Genetics and Molecular Biology(all)