Kun-Ching Lee1,2, Jai-Jen Tsai3, Chih-Wei Tseng4, Yu-Cheng Kuo5,6, Yao-Chen Chuang7, Song-Shei Lin8, Fei-Ting Hsu9,10,11. 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. Division of Gastroenterology, Department of Medicine, National Yang-Ming University Hospital, Yilan, Taiwan, R.O.C. 4. Division of Gastroenterology, Department of Internal Medicine, Dalin Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Chia-Yi, Taiwan, R.O.C. 5. Radiation Oncology, China Medical University Hospital, Taichung, Taiwan, R.O.C. 6. Department of Radiation Oncology, Show Chwan Memorial Hospital, Changhua, Taiwan, R.O.C. 7. Kiang Wu Nursing College of Macau, Macau SAR, P.R. China. 8. Department of Medical Imaging and Radiological Sciences, Central-Taiwan University of Science and Technology, Taichung, Taiwan, R.O.C. sslin@ctust.edu.tw sakiro920@tmu.edu.tw. 9. Department of Radiology, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan, R.O.C. sslin@ctust.edu.tw sakiro920@tmu.edu.tw. 10. Department of Medical Imaging, Taipei Medical University Hospital, Taipei Medical University Hospital, Taipei, Taiwan, R.O.C. 11. Research Center of Translational Imaging, College of Medicine, Taipei Medical University, Taipei, Taiwan, R.O.C.
Abstract
BACKGROUND/AIM: A previous study indicated that amentoflavone inhibits tumor growth of breast cancer. However, the anti-cancer effects and mechanism of amentoflavone in hepatocellular carcinoma (HCC) have not been elucidated. The aim of the present study was to verify the effect of amentoflavone on tumor progression in HCC. MATERIALS AND METHODS: HCC SK-Hep1 cells were treated with different concentrations of amentoflavone or 10 μM PD98059 (extracellular signal-regulated kinases (ERK) inhibitor) for 48 h, respectively, and then cell viability, NF-κB activation, levels of tumor progression-associated proteins, and cell invasion were evaluated with 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), NF-κB reporter gene assay, western blotting, and cell invasion assay. RESULTS: The results demonstrated that both amentoflavone and PD98059 not only significantly reduced cell viability, NF-κB activation, and cell invasion, but also inhibited the expression of tumor progression-associated proteins. In addition, we found that amentoflavone suppresses ERK phosphorylation. CONCLUSION: The results of the present study suggest that amentoflavone down-regulates ERK-modulated tumor progression in HCC. Copyright
BACKGROUND/AIM: A previous study indicated that amentoflavone inhibits tumor growth of breast cancer. However, the anti-cancer effects and mechanism of amentoflavone in hepatocellular carcinoma (HCC) have not been elucidated. The aim of the present study was to verify the effect of amentoflavone on tumor progression in HCC. MATERIALS AND METHODS: HCC SK-Hep1 cells were treated with different concentrations of amentoflavone or 10 μM PD98059 (extracellular signal-regulated kinases (ERK) inhibitor) for 48 h, respectively, and then cell viability, NF-κB activation, levels of tumor progression-associated proteins, and cell invasion were evaluated with 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), NF-κB reporter gene assay, western blotting, and cell invasion assay. RESULTS: The results demonstrated that both amentoflavone and PD98059 not only significantly reduced cell viability, NF-κB activation, and cell invasion, but also inhibited the expression of tumor progression-associated proteins. In addition, we found that amentoflavone suppresses ERK phosphorylation. CONCLUSION: The results of the present study suggest that amentoflavone down-regulates ERK-modulated tumor progression in HCC. Copyright