[1]卫佳,李星星,陈英华,等.β-catenin降低外源性hS100A6对骨肉瘤细胞的抑制作用[J].陆军军医大学学报(原第三军医大学学报),2010,32(16):1703-1707.
　Wei Jia,Li Xingxing,Chen Yinghua,et al.β-catenin decreases hS100A6-induced inhibition in osteosarcoma cell lines MG63 and U2OS[J].J Amry Med Univ (J Third Mil Med Univ),2010,32(16):1703-1707.
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陆军军医大学学报（原第三军医大学学报）[ISSN:1000-5404/CN:51-1095/R]

卷:
32卷
期数:
2010年第16期
页码:
1703-1707
栏目:
论著
出版日期:
2010-08-30

文章信息/Info

Title:
β-catenin decreases hS100A6-induced inhibition in osteosarcoma cell lines MG63 and U2OS
作者:
卫佳; 李星星; 陈英华; 吴丽美; 马闻; 何通川; 周兰
重庆医科大学：生物医学工程系，重庆市生物医学工程学重点实验室，重庆市超声医学工程重点实验室，省部共建国家重点实验室培育基地，医学检验系临床生化教研室，临床检验诊断学省部共建教育部重点实验室
Author(s):
Wei Jia;  Li Xingxing;  Chen Yinghua;  Wu Limei;  Ma Wen;  He Tongchuan;  Zhou Lan
State Key Laboratory of Medical Ultrasound Engineering Co-founded by Chongqing and Ministry of Science and Technology, Key Laboratory of Biomedical Engineering of Chongqing, Key Laboratory of Ultrasound Engineering in Medicine of Chongqing, Faculty of Biomedical Engineering, Key Laboratory of Medical Diagnostics of Chongqing and Ministry of Education, Faculty of Laboratory Medicine, Chongqing Medical University, Chongqing, 400016, China
关键词:
β-catenin; S100A6; 生物学作用; 骨肉瘤
Keywords:
β-catenin;  S100A6;  biological role;  osteosarcoma
分类号:
R738.1;R394.3;R73-362
文献标志码:
A
摘要:
目的    研究外源性hS100A6抑制骨肉瘤细胞作用与Wnt/β-catenin信号途径的关系。    方法    用携带人β-catenin 及其siRNA基因的重组腺病毒Adβ-catenin和AdSiβ-catenin分别上调和下调MG63和U2OS细胞中β-catenin水平，再用重组hS100A6处理这些细胞，然后通过MTT法检测细胞增殖能力的变化，Hochest染色法检测细胞凋亡的变化，划痕愈合实验和Transwell实验检测细胞迁移能力的变化。    结果    ①外源性hS100A6抑制2株骨肉瘤细胞的增殖（P<0.05）；β-catenin过表达和低表达则分别减弱和增强hS100A6对这2株细胞的增殖抑制作用（P<0.05）；②外源性hS100A6促进2株骨肉瘤细胞的凋亡（P<0.05）；β-catenin过表达和低表达则分别增强和减弱hS100A6对这2株细胞的促凋亡作用（P<0.05）；③外源性hS100A6抑制骨肉瘤细胞株MG63的迁移（P<0.05）；β-catenin过表达和低表达则分别减弱和增强hS100A6对MG63的迁移抑制作用（P<0.05）。    结论    β-catenin负性调节hS100A6对骨肉瘤的抑制作用；hS100A6对骨肉瘤的抑制作用可能经由Wnt信号途径及其他信号途径共同调控。
Abstract:

Objective  To investigate the relationship between the inhibition of hS100A6 on osteosarcoma cell lines MG63 and U2OS and Wnt/ β - catenin signaling pathway. Methods Adenoviruses carrying human β - catenin and its siRNA gene respectively were used to up - regulate and down - regulate the expression of β- catenin in MG63 and U2OS cells. Then MTT assay, Hoechst staining, scratching test and Transwell assay were used to detect cells proliferation, apoptosis and migration, respectively after the treatment of hS100A6. Results Ad β - catenin and AdSi β - catenin up - and down - regulated β - catenin expression in MG63 and U2OS ( P <0.05), respectively. Exogenous hS100A6 inhibited the proliferation of wild osteosarcoma cell lines MG63 and U2OS ( P <0 . 05), while over - or low - expression of β - catenin reduced or enhanced the inhibitive effect of S100A6 on cell proliferation respectively ( P <0 . 05). Exogenous hS100A6 promoted the apoptosis of 2 wild cell lines ( P <0 . 05), but over- or low-expression of β - catenin enhanced or reduced the ability of hS100A6 respectively ( P <0 . 05). Exogenous hS100A6 inhibited the migration of MG63 cells, however, over- or low-expression of β - catenin reduced or enhanced the ability of hS100A6 to inhibit migration ( P <0 . 05). Conclusion The inhibitory role of hS100A6 on osteosarcoma cells is regulated negatively by β - atenin. This inhibitory role may be controlled by Wnt/ β- atenin and other signaling pathways.

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更新日期/Last Update: 2010-08-31