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Chem Biol Interact. 2018 Feb 1;281:60-68. doi: 10.1016/j.cbi.2017.12.010. Epub 2017 Dec 19.

1-Hydroxy-3-[(E)-4-(piperazine-diium)but-2-enyloxy]-9,10-anthraquinone ditrifluoroactate induced autophagic cell death in human PC3 cells.

Author information

1
Graduate Institute of Clinical Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, 80708, Taiwan.
2
Institute of Biomedical Sciences, Academia Sinica, Taipei, 11529, Taiwan. Electronic address: lin0910kw@gmail.com.
3
School of Pharmacy, Kaohsiung Medical University, Kaohsiung, 80708, Taiwan.
4
Department of Medical Sciences, Tzu Chi University, Hualien, 97004, Taiwan.
5
Department of Human Development and Family Studies, National Taiwan Normal University, Taipei, 10610, Taiwan.
6
Department of Life Sciences, Tzu Chi University, Hualien, 97004, Taiwan. Electronic address: hsueyin@mail.tcu.edu.tw.
7
Institute of Biomedical Sciences, Academia Sinica, Taipei, 11529, Taiwan. Electronic address: cshih@ibms.sinica.edu.tw.

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.

KEYWORDS:

Anthraquinone derivatives; Autophagy; Prostate cancer; ROS

PMID:
29273567
DOI:
10.1016/j.cbi.2017.12.010
[Indexed for MEDLINE]

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