自噬
程序性细胞死亡
巴非霉素
细胞生物学
细胞
化学
细胞周期
蒽醌
活性氧
细胞生长
细胞周期检查点
细胞凋亡
生物
生物化学
有机化学
作者
A‐Mei Huang,Kai‐Wei Lin,Wei Lin,Li-Hung Wu,Hao‐Chun Chang,Chujun Ni,Danny Ling Wang,Hsue-Yin Hsu,Chun‐Li Su,Chiaho Shih
标识
DOI:10.1016/j.cbi.2017.12.010
摘要
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.
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