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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.
In order to investigate the molecular mechanism of FAS antibody and actinomycin D (ActD) inducing apoptosis in human cervical cancer HeLa cells, the cell viability was detected by MTT assay, the apoptosis and cell cycle were detected by flow cytometry, So as to study the effect of FAS / ActD on cell proliferation.Results showed that FAS / ActD could significantly decrease the viability of HeLa cells and induce HeLa cell apoptosis through G1 / G0 arrest and S phase arrest.In addition, Western blot analysis further Showed that FAS / ActD also caused a decrease in Bcl-2 protein expression, an increase in Bax protein expression, and a doubling in Bid protein activation, resulting in an increase in Cyto-c release in the cytoplasm, and activation plays a key role in the apoptotic process Of the caspase-9 and caspase-3.The above results suggest that the combination of FAS antibody and ActD may lead to cell cycle arrest by mitochondrial pathway, thereby inducing HeLa cell apoptosis.This study provides a new idea for the immunotherapy of cervical cancer .