摘要
目的:通过体外实验,研究缺氧对胃癌细胞侵袭转移及血管形成的影响,并初步探讨其作用机制。方法:运用3-(4,5-二甲基噻唑-2)-2,5-二苯基四氮唑溴盐(3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide,MTT)法观察缺氧对人胃癌细胞SGC-7901粘附能力的影响;选用Boyden Chamber膜侵袭系统,观察缺氧对SGC-7901游走和侵袭的影响以及诱导内皮细胞形成新生血管的影响;免疫细胞化学观察缺氧对SGC-7901细胞转化生长因子-β1(Transforming growth factor-beta1,TGF-β1)表达的影响。结果:缺氧处理后,SGC-7901细胞粘贴率增加(P<0.05),游走穿膜细胞数(167±46、196±9)或侵袭穿膜细胞数(84±5、122±8)均明显高于对照组(114±7,60±4,P<0.05),诱导内皮细胞形成管腔数(203±6.21、356±5.11)及长度(387±5.93、439±8.43)均高于对照组(129±3.45,261±6.28,P<0.05),缺氧能增加TGF-β1的表达。结论:缺氧能促进胃癌侵袭转移及血管形成。其促进侵袭转移的机制可能与增加胃癌细胞异质粘附、游走、侵袭能力有关。
Objective:To study the effect of hypoxia on the invasion ,metastasis,and angiogenesis of gastric cancer in vitro. Methods: MTT was used to study the effects of viability durng hypoxia on SGC-7901,The Boyden Chamber membrane invasion culture system was used to study invasion,metastasis,and angiogenesis. Immunocy tochemical staining was used to observe the change of TGF-β1. Resuts: In the membrane invasion culture system,the numbers of invading and migrating SGC-7901 cells were significantly higher in hypoxia group than in the control group (P〈0.05),and the numbers and length of tubes were significantly higher in hypoxia group too(P〈0.05). The adhesion rate and TGF-β1 expression were regulater in hypoxia group (P〈0.05). Conclusion:Hypoxia can inhibit the migration, invasion,and angiogenesis of SGC- 7901 gastric cancer cells in vitro. The mechanism may be regulation of TGF-β1 expression.
出处
《重庆医科大学学报》
CAS
CSCD
北大核心
2010年第6期849-852,共4页
Journal of Chongqing Medical University
基金
重庆医科大学2005年创新基金(编号:cx200504)
关键词
胃癌细胞
缺氧
侵袭转移
血管形成
转化生长因子-Β1
Gastric cancer
Hypoxia
Invasion and metastasis
Angiogenesis
Transforming growth factor-beta