1. 1-Hydroxy-3-[(E)-4-(piperazine-diium)but-2-enyloxy]-9,10-anthraquinone ditrifluoroactate induced autophagic cell death in human PC3 cells.
- Author
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Huang AM, Lin KW, Lin WH, Wu LH, Chang HC, Ni C, Wang DL, Hsu HY, Su CL, and Shih C
- Subjects
- Acetylcysteine pharmacology, Adenine analogs & derivatives, Adenine pharmacology, Anthraquinones chemical synthesis, Anthraquinones chemistry, Caspase 3 metabolism, Cell Line, Tumor, G1 Phase Cell Cycle Checkpoints drug effects, Humans, Macrolides pharmacology, Microscopy, Electron, Transmission, Microtubule-Associated Proteins metabolism, Reactive Oxygen Species metabolism, Anthraquinones toxicity, Apoptosis drug effects, Autophagy drug effects
- Abstract
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., (Copyright © 2017 Elsevier B.V. All rights reserved.)
- Published
- 2018
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