全反式维甲酸诱导胃腺癌细胞周期阻滞的作用机制  

Effects of All Trans Retinoic Acid on Cell Cycle Arrest of Gastric Carcinoma Cell Line and Its Mechanism

作　　者：杨艳梅[1] 张春艳[1] 杨悦[1] 马玉彦[1] 任丽君[1] 

机构地区：[1]哈尔滨医科大学肿瘤研究所,黑龙江哈尔滨150081

出　　处：《现代生物医学进展》2010年第13期2416-2418,共3页Progress in Modern Biomedicine

基　　金：黑龙江省教育厅科学技术研究项目(11521182);黑龙江省自然科学基金资助项目(D2007-79)

摘　　要：目的:研究全反式维甲酸(all trans retinoic acid,ATRA)对人胃腺癌细胞(SGC-7901)细胞周期阻滞的诱导作用并探讨其机制。方法:采用四甲基偶氮唑盐(MTT)方法检测ATRA对SGC-7901增殖的抑制;流式细胞术检测细胞周期,Westernblot方法检测不同浓度ATRA处理后的SGC-7901细胞中Akt、p-Ak(tSer473)、p-Ak(tThr308)、p-GSK-3β(Ser9)和cyclinD1的表达情况。结果:10-9～10-5mol/L的ATRA作用SGC-7901细胞48h,能显著抑制细胞增殖,其抑制率分别为10.2%±0.5%、15.3%±0.5%、17.0%±0.7%、28.4%±1.0%和36.9%±0.7%;G1期细胞比率随着ATRA浓度的增加而增加,呈明显的G1期阻滞;Westernblot检测显示ATRA对细胞中Akt蛋白的表达没有明显影响,两种p-Akt蛋白的表达显著下调,ATRA显著降低细胞中cyclinD1和p-GSK-3β的表达。结论:ATRA可能通过抑制磷酸化Akt蛋白表达而减少p-GSK-3β的表达,从而减少cyclinD1的表达量,进而诱导SGC-7901细胞发生G1期阻滞。Objective：To investigate the effects of all trans retinoic acid（ATRA） on cell cycle arrest of human gastric carcinoma cell line（SGC-7901） and its mechanism.Methods：The effects of ATRA on the cell proliferation was detected by methyl thiazolyl tetrazolium（MTT）,cell cycle was detected by flow cytometry,and the expression of Akt,p-Akt（Ser473）,p-Akt（Thr308）,P-GSK-3β（Ser9） and cyclin D1 were measured by Western blot.Results：SGC-7901 cells were exposed to 10-9-10-5mol/L ATRA for 48 hours,and the inhibitory rate was 10.2%±0.5%,15.3%±0.5%,17.0%±0.7%,28.4%±1.0% and 36.9%±0.7%,respectively.The proportion of SGC-7901 cells at G1 phase increased significantly with the increasing of the ATRA concentration,which showed apparent G1 phase arrest.ATRA did not influence the expression of Akt,but decreased the expression of p-Akt（Ser473） and p-Akt（Thr308）;ATRA significantly decreased the expression of cyclin D1 and p-GSK-3β.Conclusion：ATRA could induce G1 phase arrest by decreasing the expression of p-Akt（Ser473） and p-Akt（Thr308）,and the subsequent suppression of p-GSK-3βand cyclin D1.

关 键 词：全反式维甲酸 胃癌 Akt CYCLIND1 GSK-3Β 

分 类 号：R735.2[医药卫生—肿瘤]