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

A. Mei Huang, Kai Wei Lin, Wei Hong Lin, Li Hung Wu, Hao Chun Chang, Chujun Ni, Danny Ling Wang, Hsue Yin Hsu, Chun Li Su, Chiaho Shih

Research output: Contribution to journalArticle

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.

Original languageEnglish
Pages (from-to)60-68
Number of pages9
JournalChemico-Biological Interactions
Volume281
DOIs
Publication statusPublished - 2018 Feb 1

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Autophagy
Cell death
Reactive Oxygen Species
Cells
Acetylcysteine
Anthraquinones
Microtubule-Associated Proteins
G1 Phase
Cell growth
G1 Phase Cell Cycle Checkpoints
9,10-anthraquinone
piperazine
G2 Phase
S Phase
Cell Division
Prostatic Neoplasms
Cell Death
Growth
Population

Keywords

  • Anthraquinone derivatives
  • Autophagy
  • Prostate cancer
  • ROS

ASJC Scopus subject areas

  • Toxicology

Cite this

1-Hydroxy-3-[(E)-4-(piperazine-diium)but-2-enyloxy]-9,10-anthraquinone ditrifluoroactate induced autophagic cell death in human PC3 cells. / Huang, A. Mei; Lin, Kai Wei; Lin, Wei Hong; Wu, Li Hung; Chang, Hao Chun; Ni, Chujun; Wang, Danny Ling; Hsu, Hsue Yin; Su, Chun Li; Shih, Chiaho.

In: Chemico-Biological Interactions, Vol. 281, 01.02.2018, p. 60-68.

Research output: Contribution to journalArticle

Huang, A. Mei ; Lin, Kai Wei ; Lin, Wei Hong ; Wu, Li Hung ; Chang, Hao Chun ; Ni, Chujun ; Wang, Danny Ling ; Hsu, Hsue Yin ; Su, Chun Li ; Shih, Chiaho. / 1-Hydroxy-3-[(E)-4-(piperazine-diium)but-2-enyloxy]-9,10-anthraquinone ditrifluoroactate induced autophagic cell death in human PC3 cells. In: Chemico-Biological Interactions. 2018 ; Vol. 281. pp. 60-68.
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AU - Huang, A. Mei

AU - Lin, Kai Wei

AU - Lin, Wei Hong

AU - Wu, Li Hung

AU - Chang, Hao Chun

AU - Ni, Chujun

AU - Wang, Danny Ling

AU - Hsu, Hsue Yin

AU - Su, Chun Li

AU - Shih, Chiaho

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AB - 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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