摘要
目的:初步探讨Smad7基因对肺癌细胞生长的影响。方法:设实验组和对照组。实验组以携带Smad7cDNA的重组腺病毒载体Ad Smad7转染A549细胞,对照组以空腺病毒载体转染A549细胞。转染后,2组培养基中分别加入TGFβ1继续培养。观察2组A549细胞培养12d后的克隆形成率,培养第1d、3d、5d、7d的存活细胞数和培养第7d的细胞周期。结果:实验组细胞生长速率高于对照组(P<0.05);实验组克隆形成率(34±7)%高于对照组的(13±3)%(t=10.674,P<0.01);实验组G0/G1期细胞比例0.67±0.16,低于对照组的0.79±0.11(t=4.836,P<0.05);S期细胞比例0.19±0.02,高于对照组的0.06±0.01(t=15.357,P<0.01)。结论:Smad7参与了肺癌细胞内的TGFβ信号通路,它可以阻断TGFβ对肺癌细胞的生长抑制作用。
Aim : To identify the effect of smad7 transfection on cell proliferation of lung cancer cell line A549. Mothods: Recombinant adenovirus vector encoding Smad7 (Ad-Smad7) and mock-adenovirus vector were transfected into A549 cell, and named Smad7-A549 and mock-A549, respectively. The two kind of cells were cultured with TGFβ1 for 1d, 3d, 5d, 7d, and the survival cells were counted, the clone-formation rate on the 12th d and cell cycle on the 7th d were detected. Results: Compared with mock-A549, speed of Smad7-A549 proliferation was faster( P 〈0. 05 ) , clone-formation rate and propotion of S phase cell were higher (P 〈0. 05 ) , and propotion of G0/G1 phase cell were lower. Conclusion: Smad7 participates in the signal pathway of TGFβ in lung cancer cell. Smad7 may block the inhibition of TGFβ to proliferation.
出处
《郑州大学学报(医学版)》
CAS
北大核心
2006年第3期525-527,共3页
Journal of Zhengzhou University(Medical Sciences)