Chun-Min Su1, Chi-Huan Li2, Meng-Chu Huang3, Po-Fu Yueh4,5, Fei-Ting Hsu4, Rong-Fong Lin6, Li-Cho Hsu7. 1. Department of Surgery, Show Chwan Memorial Hospital, Changhua, Taiwan, R.O.C. 2. Department of Orthopedics, Chang Bing Show Chwan Memorial Hospital, Changhua, Taiwan, R.O.C. 3. Department of Medical Imaging, Show Chwan Memorial Hospital, Changhua, Taiwan, R.O.C. 4. Department of Biological Science and Technology, China Medical University, Taichung, Taiwan, R.O.C. 5. Institute of Traditional Medicine, School of Medicine, National Yang Ming Chiao Tung University, Taipei, Taiwan, R.O.C. 6. Department of Optometry, Central Taiwan University of Science and Technology, Taichung, Taiwan, R.O.C. 7. Department of Medicine, National Yang-Ming Chiao-Tung University Hospital, Yilan, Taiwan, R.O.C. hsulc@ymuh.ym.edu.tw.
Abstract
BACKGROUND/AIM: Sorafenib has been reported to show anti-osteosarcoma (anti-OS) efficacy by inhibiting metastasis; however, a phase II trial suggested that further combination with other agents could be necessary to achieve permanent remission. Herein, we aimed to identify whether amentoflavone, an abundant natural bioflavonoid found in many medicinal plants, can improve the treatment efficacy of sorafenib in OS. MATERIALS AND METHODS: Cell viability, metastasis, apoptosis, and nuclear translocation of NF-κB after amentoflavone combined with sorafenib were assayed by MTT, transwell migration/invasion, western blotting, flow cytometry, and immunofluorescence staining, respectively. RESULTS: The sorafenib-induced cytotoxicity and apoptosis of U-2 OS was enhanced by combining treatment with QNZ (NF-κB inhibitor) or amentoflavone. NF-κB nuclear translocation, NF-κB phosphorylation, and metastasis capacity of U-2 OS cells were inhibited by amentoflavone combined with sorafenib. CONCLUSION: Amentoflavone may sensitize OS to sorafenib treatment by inducing intrinsic and extrinsic apoptosis and inhibiting ERK/NF-κB signaling transduction.
BACKGROUND/AIM: Sorafenib has been reported to show anti-osteosarcoma (anti-OS) efficacy by inhibiting metastasis; however, a phase II trial suggested that further combination with other agents could be necessary to achieve permanent remission. Herein, we aimed to identify whether amentoflavone, an abundant natural bioflavonoid found in many medicinal plants, can improve the treatment efficacy of sorafenib in OS. MATERIALS AND METHODS: Cell viability, metastasis, apoptosis, and nuclear translocation of NF-κB after amentoflavone combined with sorafenib were assayed by MTT, transwell migration/invasion, western blotting, flow cytometry, and immunofluorescence staining, respectively. RESULTS: The sorafenib-induced cytotoxicity and apoptosis of U-2 OS was enhanced by combining treatment with QNZ (NF-κB inhibitor) or amentoflavone. NF-κB nuclear translocation, NF-κB phosphorylation, and metastasis capacity of U-2 OS cells were inhibited by amentoflavone combined with sorafenib. CONCLUSION: Amentoflavone may sensitize OS to sorafenib treatment by inducing intrinsic and extrinsic apoptosis and inhibiting ERK/NF-κB signaling transduction.
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