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Amentoflavone Inhibits Hepatocellular Carcinoma Progression Through Blockage of ERK/NF-ĸB Activation.

AbstractAIM:
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.
AuthorsKun-Ching Lee, Wei-Ting Chen, Yu-Chang Liu, Song-Shei Lin, Fei-Ting Hsu
JournalIn vivo (Athens, Greece) (In Vivo) 2018 Sep-Oct Vol. 32 Issue 5 Pg. 1097-1103 ISSN: 1791-7549 [Electronic] Greece
PMID30150431 (Publication Type: Journal Article)
CopyrightCopyright© 2018, International Institute of Anticancer Research (Dr. George J. Delinasios), All rights reserved.
Chemical References
  • Antineoplastic Agents
  • Biflavonoids
  • NF-kappa B
  • amentoflavone
  • Extracellular Signal-Regulated MAP Kinases
Topics
  • Animals
  • Antineoplastic Agents (pharmacology)
  • Biflavonoids (pharmacology)
  • Carcinoma, Hepatocellular (drug therapy, metabolism, pathology)
  • Cell Line, Tumor
  • Disease Models, Animal
  • Disease Progression
  • Extracellular Signal-Regulated MAP Kinases (metabolism)
  • Genes, Reporter
  • Humans
  • Immunohistochemistry
  • Liver Neoplasms (drug therapy, metabolism, pathology)
  • Mice
  • Molecular Imaging
  • NF-kappa B (metabolism)
  • Signal Transduction (drug effects)
  • Tumor Burden (drug effects)
  • Xenograft Model Antitumor Assays

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