Bel-7402细胞通过自噬逃避FAS/ActD诱导的凋亡

为了探究FAS抗体与放线菌素D（actinomycin D,ActD）诱导肝癌细胞Bel-7402凋亡的作用机制，通过自噬阻断剂3-MA的作用，来探讨自噬与凋亡的关系.利用电子显微镜和流式细胞仪观察细胞自噬及凋亡.结果表明，FAS/ActD在诱导细胞凋亡的同时伴有细胞自噬现象，在3-MA作用下,FAS/ActD所诱导的细胞自噬体减少,而凋亡现象严重.并且通过流式细胞仪分析表明，3-MA明显增高FAS/ActD所诱导的细胞凋亡率. Western印迹分析进一步显示,FAS/ActD能引起caspase-3激活产生断裂，同时刺激LC3和BECN1表达,而3-MA作用后自噬体减少，同时LC3和BECN1表达降低，但是caspase-3断裂带表达明显增加.以上结果提示，FAS/ActD诱导的Bel-7402细胞凋亡的同时伴有细胞自噬，Bel-7402细胞通过自噬逃避FAS/ActD诱导的凋亡.

Autophagy Protects Bel-7402 Cells from Apoptosis Induced by FAS/ActD

To investigate the effect of autophagy on FAS/ActD-induced apoptosis in Bel-7402 cells, autophagy blocker 3-MA was used. Cell apoptosis and activation of autophagy were detected by electron microscopy and flow cytometry. The results showed that FAS/ActD induced apoptosis of Bel-7402 cells. 3-MA reduced the number of autophgosomes and increased apoptotic cells. Western blot analysis showed that FAS/ActD activated caspase-3 with increased expression of LC3 and BECN1.3-MA significantly suppressed LC3 and BECN1 expression and increased the 17 kD caspase-3 fragment. These results suggested that FAS/ActD induced both cell apoptosis and autophagy; the latter might help the cells to escape from apoptotic cell death.