摘要
目的研究全反式维A酸(ATRA)诱导肺鳞癌细胞株A2凋亡作用并初步探讨其作用机制,寻找肺癌治疗的新途径。方法体外培养A2细胞,随机分为两组,实验组加ATRA使其终浓度为5μmol/L,对照组加入二甲亚砜使其终浓度为0.1%,继续培养48 h后用流式细胞仪技术分别检测Rb、p53基因表达率,同时用DNA凋亡分析法检测肿瘤细胞凋亡发生率,研究三者之间的相关关系。结果A2细胞实验组中细胞凋亡发生率显著增高(P<0.01),Rb和p53基因表达率显著增强(P<0.01)。A2细胞中凋亡发生率与Rb基因表达率之间正相关(P<0.05),与p53基因表达率之间亦呈正相关关系(P<0.05)。结论ATRA可能通过上调Rb和p53基因表达途径使A2细胞阻滞在G0/G1期,进而诱导肺癌细胞A2凋亡。
Objective To investigate the interrelationship between apoptosis of human lung carcinoma cell line A2 and its expression of Rb, p53 gene proteins induced by ATRA, and to evaluate the mechanism. Methods In vitro, A2 cell line is divided into two groups at random, with Group A treated with 5μmol/L ATRA and Group B with 0.1% Dimethylsulfoxid. After 48 hours ofincubation, the apoptosis and Rb, p53 gene expressions were observed with FACS technique. Results In Group A of A2 cells, the apoptosis induced by ATRA increased prominently（P 〈 0.01）. The expressions of Rb and p 5 3 gene protein were induced by ATRA enhanced prominently （ P 〈 0.01 ）. There was positive corelationship between p53 gene and the rate of cancer cell apotosis（P = 0. 028）, and also positive corelationship between p53 gene and the rate of cancer cell apotosis（P = 0. 019）. Conclusion ATRA can arrest cells in G0/G1 status by Rb and p53 up-regulation, and then induce lung cancer cells A2 apoptosis.
出处
《实用临床医药杂志》
CAS
2006年第1期41-43,共3页
Journal of Clinical Medicine in Practice
