Amentoflavone inhibits hepatocellular carcinoma progression through blockage of ERK/NF-κB activation

Kun Ching Lee, Wei Ting Chen, Yu Chang Liu, Song Shei Lin, Fei Ting Hsu

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5 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)1097-1103
Number of pages7
JournalIn Vivo
Volume32
Issue number5
DOIs
Publication statusPublished - Sep 1 2018

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Keywords

  • Amentoflavone
  • Bioluminescence imaging
  • Extracellular signal-regulated kinase
  • Hepatocellular carcinoma
  • Nuclear factor-kappaB

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)
  • Pharmacology

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