Yen-Ju Lee1,2, Jing-Gung Chung3,4, Yi-Ting Chien5, Song-Shei Lin6, Fei-Ting Hsu7. 1. Department of Emergency Medicine, Zuoying Branch of Kaohsiung Armed Forces General Hospital, Kaohsiung, Taiwan, R.O.C. 2. Department of Medical Imaging and Radiological Sciences, Central-Taiwan University of Science and Technology, Taichung, Taiwan, R.O.C. 3. Department of Biological Science and Technology, China Medical University, Taichung, Taiwan, R.O.C. 4. Department of Biotechnology, Asia University, Taichung, Taiwan, R.O.C. 5. Department of Medical Imaging and Radiology, Shu-Zen Junior College of Medicine and Management, Kaohsiung, Taiwan, R.O.C. 6. 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. 7. Department of Biological Science and Technology, China Medical University, Taichung, Taiwan, R.O.C. sslin@ctust.edu.tw sakiro920@gmail.com.
Abstract
BACKGROUND/AIM: Amentoflavone has been implicated in reducing the metastatic potential of osteosarcoma (OS) cells in vitro. The aim of the present study was to verify the antitumoral efficacy and the potential mechanism of amentoflavone osteosarcoma progression inhibition in vivo. MATERIALS AND METHODS: A U-2 OS osteosarcoma xenograft mouse model was used in this study. Mice were treated with a vehicle control or amentoflavone (100 mg/kg/day) for 15 days. Tumor growth, signal transduction, and expression of tumor progression-associated proteins were evaluated using a digital caliper, bioluminescence imaging (BLI), animal computed tomography (CT), and ex vivo western blotting assay. RESULTS: Amentoflavone significantly inhibits tumor growth and reduces protein levels of phospho-extracellular signal-regulated kinase (P-ERK), nuclear factor-kappaB (NF-κB) p65 (Ser536), vascular endothelial growth factor (VEGF), matrix metallopeptidase 9 (MMP-9), X-linked inhibitor of apoptosis protein (XIAP), and cyclin-D1 in osteosarcoma in vivo. CONCLUSION: The inhibition of ERK/NF-κB activation is associated with amentoflavone-inhibited osteosarcoma progression in vivo. Copyright
BACKGROUND/AIM: Amentoflavone has been implicated in reducing the metastatic potential of osteosarcoma (OS) cells in vitro. The aim of the present study was to verify the antitumoral efficacy and the potential mechanism of amentoflavone osteosarcoma progression inhibition in vivo. MATERIALS AND METHODS: A U-2 OS osteosarcoma xenograftmouse model was used in this study. Mice were treated with a vehicle control or amentoflavone (100 mg/kg/day) for 15 days. Tumor growth, signal transduction, and expression of tumor progression-associated proteins were evaluated using a digital caliper, bioluminescence imaging (BLI), animal computed tomography (CT), and ex vivo western blotting assay. RESULTS:Amentoflavone significantly inhibits tumor growth and reduces protein levels of phospho-extracellular signal-regulated kinase (P-ERK), nuclear factor-kappaB (NF-κB) p65 (Ser536), vascular endothelial growth factor (VEGF), matrix metallopeptidase 9 (MMP-9), X-linked inhibitor of apoptosis protein (XIAP), and cyclin-D1 in osteosarcoma in vivo. CONCLUSION: The inhibition of ERK/NF-κB activation is associated with amentoflavone-inhibited osteosarcoma progression in vivo. Copyright