TY - JOUR
T1 - Amentoflavone inhibits hepatocellular carcinoma progression through blockage of ERK/NF-κB activation
AU - Lee, Kun Ching
AU - Chen, Wei Ting
AU - Liu, Yu Chang
AU - Lin, Song Shei
AU - Hsu, Fei Ting
N1 - Funding Information:
The project was supported by the National Health Research Institutes and Taipei Medical University Hospital (grant no. MG-105-SP-07 and MG-106-SP-07). This study was also supported by grants RD2017-016 (National Yang-Ming University Hospital, Yilan, Taiwan) and CTU106-P-16 (Central-Taiwan University of Science and Technology, Taichung, Taiwan). The Authors acknowledge the technical services provided by Clinical Medicine Research Laboratory of National Yang-Ming University Hospital. We would also like to thank Translational Laboratory, Department of Medical Research, Taipei Medical University Hospital, Taipei, Taiwan for equipment support.
Publisher Copyright:
© 2018 Institute of Electrical and Electronics Engineers Inc. All rights reserved.
Copyright:
Copyright 2018 Elsevier B.V., All rights reserved.
PY - 2018/9/1
Y1 - 2018/9/1
N2 - 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.
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) 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.
KW - Amentoflavone
KW - Bioluminescence imaging
KW - Extracellular signal-regulated kinase
KW - Hepatocellular carcinoma
KW - Nuclear factor-kappaB
KW - Amentoflavone
KW - Bioluminescence imaging
KW - Extracellular signal-regulated kinase
KW - Hepatocellular carcinoma
KW - Nuclear factor-kappaB
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U2 - 10.21873/invivo.11351
DO - 10.21873/invivo.11351
M3 - Article
C2 - 30150431
AN - SCOPUS:85053027976
SN - 0258-851X
VL - 32
SP - 1097
EP - 1103
JO - In Vivo
JF - In Vivo
IS - 5
ER -