摘要
为了探讨FAS抗体与放线菌素D(actinomycin D,ActD)联合作用诱导人宫颈癌HeLa细胞凋亡的分子机制,通过MTT法检测细胞活力,利用流式细胞仪检测细胞凋亡和细胞周期,从而研究FAS/ActD抑制细胞增殖的作用.结果表明,FAS/ActD能明显降低HeLa细胞的活力,并且通过G1/G0期阻滞和S期阻滞诱导HeLa细胞凋亡.此外,Western印迹分析进一步显示,FAS/ActD还能引起Bcl-2蛋白表达降低,Bax蛋白表达增加,Bid蛋白发生断裂激活,导致细胞质中Cyto-c释放的增加,并激活在细胞凋亡的执行过程中起着关键作用的caspase-9和caspase-3.以上结果提示,FAS抗体与ActD的联合作用可能经线粒体途径引起细胞周期阻滞,从而诱导HeLa细胞凋亡.该研究为宫颈癌的免疫治疗提供了新的思路.
To investigate the apoptosis induced by FAS/ActD （actinomycin D） in HeLa cells, MTT and flow cytometry were used to detected the cell viability and cell cycle changes were underlined. The results showed that FAS/ActD significantly induced apoptosis and reduced the viability of cells with the arrest in G1/G0 phase and S phase. Western blot analysis showed that decreased Bcl-2 and increased Bax expression following the treatment if FAS/ActD of the cleavage of Bid protein coordinated with increased Cyto-c cytoplasmic release, and the activation of caspase-9 and -3. These results suggested that FAS antibody might be applied with ActD to arrest cell cycle and induced apoptosis by the mitochondrial apoptotic pathway.
出处
《中国生物化学与分子生物学报》
CAS
CSCD
北大核心
2014年第6期597-603,共7页
Chinese Journal of Biochemistry and Molecular Biology
基金
黑龙江省教育厅科学技术研究项目(No.12521616)~~
