Asian Pacific Journal of Cancer Prevention

Asian Pacific Journal of Cancer Prevention (아시아태평양암예방학회)
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Effects of Aloe-emodin and Emodin on Proliferation of the MKN45 Human Gastric Cancer Cell Line

  • Chihara, Takeshi (Division of Biochemistry, Fujita Memorial Nanakuri Institute, Fujita Health University) ;
  • Shimpo, Kan (Division of Biochemistry, Fujita Memorial Nanakuri Institute, Fujita Health University) ;
  • Beppu, Hidehiko (Division of Biochemistry, Fujita Memorial Nanakuri Institute, Fujita Health University) ;
  • Yamamoto, Naoki (Laboratory of Molecular Biology & Histochemistry, Fujita Health University Joint Research Laboratory) ;
  • Kaneko, Takaaki (Division of Biochemistry, Fujita Memorial Nanakuri Institute, Fujita Health University) ;
  • Wakamatsu, Kazumasa (Department of Chemistry, Fujita Health University School of Health Sciences) ;
  • Sonoda, Shigeru (Division of Biochemistry, Fujita Memorial Nanakuri Institute, Fujita Health University)
  • Published : 2015.05.18
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Abstract

Aloe-emodin (1, 8-dihydroxy-3-hydroxyl-methylanthraquinone; AE) and emodin (1,3,8-trihydroxy-6-methylanthraquinone; EM) are anthraquinone derivatives that have been detected in some medical plants and share similar anthraquinone structures. AE and EM have been shown to exhibit anticancer activities in various cancer cell lines; however, the inhibitory effects of these derivatives on the growth of cancer cells were previously reported to be different. Gastric cancer is the second most common cause of cancer cell death worldwide. In the present study, we examined the inhibitory effects of 0.05 mM AE and 0.05 mM EM on the proliferation of the MKN45 human gastric cancer cell line. The proliferation of MKN45 cells was significantly inhibited in AE- and EM-treated groups 24 h and 48 h after treatment. Furthermore, the inhibitory effects of EM were stronger than those of AE. The cell cycle of MKN45 cells were arrested in G0/G1 phase or G0/G1 and G2/M phases by AE and EM, respectively. However, an analysis of intracellular polyamine levels and DNA fragmentation revealed that the mechanisms underlying cell death following cell arrest induced by AE and EM differed.

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