The autophagy of human prostate cancer cells (PC3 cells) induced by a new anthraquinone derivative, 1-Hydroxy-3-[(E)-4-(piperazine-diium)but-2-enyloxy]-9,10-anthraquinone ditrifluoroactate (PA) was investigated, and the relationship between autophagy and reactive oxygen species (ROS) generation was studied.

The results indicated that PA induced PC3 cell death in a time- and dose-dependent manner, could inhibit PC3 cell growth by G1 phase cell cycle arrest and corresponding decrease in the G2/M cell population and induced S-phase arrest accompanied by a significant decrease G2/M and G1 phase numbers after PC3 cells treated with PA for 48 h, and increased the accumulation of autophagolysosomes and microtubule-associated protein LC3-ll, a marker of autophagy. However, these phenomenon were not observed in the group pretreated with the autophagy inhibitor 3-MA or Bafilomycin A1 (BAF), suggesting that PA induced PC3 cell autophagy. In addition, we found that PA triggered ROS generation in cells, while the levels of ROS decreased in the N-acetylcysteine (NAC) co-treatment, indicating that PA-mediated autophagy was partly blocked by NAC. In summary, the autophagic cell death of human PC3 cells mediated by PA-triggered ROS generation.

一种新的蒽醌衍生物1-Hydroxy-3-[（E）-4-（piperazine-diium）but-2-enyloxy] -9,10-anthraquinone ditrifluoroactate （）诱导的人前列腺癌细胞（PC3细胞）的自噬。PA），并研究了自噬与活性氧（ROS）生成之间的关系。

结果表明，PA诱导PC3细胞死亡具有时间和剂量依赖性，可以通过G1期细胞周期停滞以及相应的G2 / M细胞数量减少和S期停滞伴随着显着抑制PC3细胞的生长。降低PA3处理PC3细胞48 h后的G2 / M和G1期数，并增加自噬体和微管相关蛋白LC3-II（自噬的标志物）的积累。但是，在用自噬抑制剂3-MA或Bafilomycin A1（BAF）预处理的组中未观察到这些现象，表明PA诱导了PC3细胞自噬。此外，我们发现PA触发了细胞中ROS的生成，而N-乙酰半胱氨酸（NAC）协同处理中ROS的水平降低，表明PA介导的自噬被NAC部分阻止。总之，