ERK/NF-κB激活的抑制与穗花杉双黄酮抑制骨肉瘤进展相关。
Suppression of ERK/NF-κB Activation Is Associated With Amentoflavone-Inhibited Osteosarcoma Progression .
作者信息
Lee Yen-Ju, Chung Jing-Gung, Chien Yi-Ting, Lin Song-Shei, Hsu Fei-Ting
机构信息
Department of Emergency Medicine, Zuoying Branch of Kaohsiung Armed Forces General Hospital, Kaohsiung, Taiwan, R.O.C.
Department of Medical Imaging and Radiological Sciences, Central-Taiwan University of Science and Technology, Taichung, Taiwan, R.O.C.
出版信息
Anticancer Res. 2019 Jul;39(7):3669-3675. doi: 10.21873/anticanres.13515.
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.
背景/目的：在体外实验中，穗花杉双黄酮已被证实可降低骨肉瘤（OS）细胞的转移潜能。本研究旨在验证穗花杉双黄酮在体内对骨肉瘤进展的抗肿瘤疗效及潜在机制。
材料与方法
本研究采用U-2 OS骨肉瘤异种移植小鼠模型。小鼠分别接受溶媒对照或穗花杉双黄酮（100 mg/kg/天）治疗15天。使用数字卡尺、生物发光成像（BLI）、动物计算机断层扫描（CT）和离体蛋白质免疫印迹分析评估肿瘤生长、信号转导及肿瘤进展相关蛋白的表达。
结果
在体内实验中，穗花杉双黄酮可显著抑制骨肉瘤的肿瘤生长，并降低磷酸化细胞外信号调节激酶（P-ERK）、核因子-κB（NF-κB）p65（Ser536）、血管内皮生长因子（VEGF）、基质金属蛋白酶9（MMP-9）、X连锁凋亡抑制蛋白（XIAP）和细胞周期蛋白D1的蛋白水平。
结论
ERK/NF-κB激活的抑制与穗花杉双黄酮在体内抑制骨肉瘤进展相关。
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