Kun-Ching Lee1,2, Wei-Ting Chen1,3, Yu-Chang Liu1,2, Song-Shei Lin4, Fei-Ting Hsu5,6,7,8. 1. Department of Medical Imaging and Radiological Sciences, Central-Taiwan University of Science and Technology, Taichung, Taiwan, R.O.C. 2. Department of Radiation Oncology, National Yang-Ming University Hospital, Yilan, Taiwan, R.O.C. 3. Department of Psychiatry, Zuoying Branch of Kaohsiung Armed Forces General Hospital, Kaohsiung, Taiwan, R.O.C. 4. Department of Medical Imaging and Radiological Sciences, Central-Taiwan University of Science and Technology, Taichung, Taiwan, R.O.C. sslin@ctust.edu.tw sakiro920@gmail.com. 5. Department of Radiology, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan, R.O.C. sslin@ctust.edu.tw sakiro920@gmail.com. 6. Department of Medical Imaging, Taipei Medical University Hospital, Taipei, Taiwan, R.O.C. 7. Research Center of Translational Imaging, College of Medicine, Taipei Medical University, Taipei, Taiwan, R.O.C. 8. Graduate Institute of Cancer Biology and Drug Discovery, College of Medical Science and Technology, Taipei Medical University, Taipei, Taiwan, R.O.C.
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) 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. Copyright
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. Copyright
Authors: Henning Schulze-Bergkamen; Binje Fleischer; Marcus Schuchmann; Achim Weber; Arndt Weinmann; Peter H Krammer; Peter R Galle Journal: BMC Cancer Date: 2006-10-02 Impact factor: 4.430