缓激肽促进人肺腺癌细胞株A549的侵袭及其机制  

Effect of bradykinin on human lung cancer cell line A549 migration and invasion ability

作　　者：胡伟[1] 胡祎[2] 周昆[1] 夏宗江[1] 王跃斌[1] 

机构地区：[1]郑州大学第一附属医院胸外科,450052 [2]中山大学肿瘤防治中心胸科

出　　处：《中华实验外科杂志》2011年第7期1166-1168,共3页Chinese Journal of Experimental Surgery

摘　　要：目的观察缓激肽（BK）对人肺癌细胞株A549迁移、侵袭能力的影响。方法应用划痕愈合实验和Transwell实验检测BK对40例人肺癌细胞株A549的划痕愈合和运动侵袭能力。通过Western blot分析刺激和抑制缓激肽各20例后基质金属蛋白酶（MMP）-2、MMP-9和E-钙黏素（E-Cadherin）的变化并研究其机制。结果划痕实验后分别测量愈合距离，结果示BK组24h和48h后迁移细胞数分别为69．2±3．3、94．1±2．9，而阻断其受体或者ERK1／2通路则迁移细胞数分别为51．2±2．1、73．2±2．7和47．5±3．4、77．6±3．8。Transwell实验检测BK对A549侵袭能力的影响结果显示BK可以明显促进A549的侵袭能力。阻断BK受体或ERK1／2通路则可以抑制其侵袭能力。结论缓激肽促进人肺腺癌细胞株A549的迁移和侵袭能力。Objective To investigate the effect of bradykinin （BK） on human lung cancer cell line A549 migration,invasion ability. Methods Scratch Healing and Transwell assay of bradykinin were used to detect scratch healing and movement on ？,549 human lung cancer cells. Analysis the changes of matrix metalloproteinase （MMP）-2, MMP-9 and E-Cadherin after stimulate and suppress 20 cases respectively in the aim to describe the mechanism by Western blotting. Results In the former, BK group promote cell migration significantly, migrated cell was 69.2 ± 3.3, 94. 1 ±2. 9 respectively after 24 h and 48 h,blocking its receptor or ERK1/2 pathway inhibit migration, migrated cell was 51.2 ±2. 1, 73.2 ±2. 7 and 47.5 ±3.4,77.6 ±3.8 after 24 h and 48 h. In the latter,Transwell assay of A549 BK showed invasion of A549 BK can significantly promote the invasion ability of A549 to penetrate the basement membrane of the cell. And blocking BK receptor or ERK1/2 pathway can inhibit the invasion. Conclusion Bradykinin promote human lung adenocarcinoma cell line A549 migration and invasion.

关 键 词：缓激肽 肺癌细胞 迁移 侵袭 

分 类 号：R734.2[医药卫生—肿瘤]