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.
| Original language | English |
|---|---|
| Pages (from-to) | 3887-3891 |
| Number of pages | 5 |
| Journal | Asian Pacific Journal of Cancer Prevention |
| Volume | 16 |
| Issue number | 9 |
| DOIs | |
| Publication status | Published - 01-01-2015 |
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All Science Journal Classification (ASJC) codes
- Epidemiology
- Oncology
- Public Health, Environmental and Occupational Health
- Cancer Research
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Effects of aloe-emodin and emodin on proliferation of the MKN45 human gastric cancer cell line. / Chihara, Takeshi; Shimpo, Kan; Beppu, Hidehiko; Yamamoto, Naoki; Kaneko, Takaaki; Wakamatsu, Kazumasa; Sonoda, Shigeru.
In: Asian Pacific Journal of Cancer Prevention, Vol. 16, No. 9, 01.01.2015, p. 3887-3891.Research output: Contribution to journal › Article
TY - JOUR
T1 - Effects of aloe-emodin and emodin on proliferation of the MKN45 human gastric cancer cell line
AU - Chihara, Takeshi
AU - Shimpo, Kan
AU - Beppu, Hidehiko
AU - Yamamoto, Naoki
AU - Kaneko, Takaaki
AU - Wakamatsu, Kazumasa
AU - Sonoda, Shigeru
PY - 2015/1/1
Y1 - 2015/1/1
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=84930165041&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84930165041&partnerID=8YFLogxK
U2 - 10.7314/APJCP.2015.16.9.3887
DO - 10.7314/APJCP.2015.16.9.3887
M3 - Article
VL - 16
SP - 3887
EP - 3891
JO - Asian Pacific Journal of Cancer Prevention
JF - Asian Pacific Journal of Cancer Prevention
SN - 1513-7368
IS - 9
ER -