TY - JOUR
T1 - Conjugated docosahexaenoic acid is a potent inducer of cell cycle arrest and apoptosis and inhibits growth of colo 201 human colon cancer cells
AU - Danbara, Naoyuki
AU - Yuri, Takashi
AU - Tsujita-Kyutoku, Miki
AU - Sato, Mutsuya
AU - Senzaki, Hideto
AU - Takada, Hideho
AU - Hada, Takahiko
AU - Miyazawa, Teruo
AU - Okazaki, Kazuichi
AU - Tsubura, Airo
N1 - Funding Information:
The authors thank Ms. T. Akamatsu for her excellent technical assistance and Ms. Y. Yoshida for preparing the manuscript. This work was supported in part by a Health and Labor Science Research Grant for Research on Risk of Chemical Substances from the Ministry of Health, Labor and Welfare, Japan. Address correspondence to A. Tsubura, Department of Pathology II, Kansai Medical University, Moriguchi, Osaka 570–8506, Japan. Phone: +81– 6–6993–9431. FAX: +81–6–6992–5023. E-mail: tsubura@ takii.kmu.ac.jp.
PY - 2004
Y1 - 2004
N2 - The effect of conjugated docosahexaenoic acid (CDHA) on the inhibition of colon cancer cell growth was examined iyn the colo 20I human colon cancer cell line, and the effect was compared with docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA). CDHA was a more potent tumor cell growth inhibitor than DHA and EPA by colorimetric 3-(4,5-dimethylthiazol-2-yl)-5-(3y- carboxymethoxyphenyl)-2 -(4-sulfophenyl)-2H-tetrazolium (MTS) assay (IC 50for 72 h: 31.6 μM, 46.8 μM, and 56.6 μM, respectively). CDHA inhibited cell cycle progression, due to accumulation of cells in G1 phase, which involved increased p21Cip1/Waf1and decreased cyclin D1, cyclin E, and proliferating cell nuclear antigen expression; the p53 and cyclin A levels were unchanged. Induction of apoptosis was confirmed by the appearance of sub-G1 populations, and apoptosis cascade involved upregulation of the apoptosis-enhancing proteins (Bak and Bcl-xS) and downregulation of the apoptosis-suppressing proteins (Bcl-xL and Bcl-2). CDHA modulated cell cycle regulatory proteins and apoptosis-related proteins, similar to the effects of DHA. CDHA at a dietary dose of 1.0% significantly inhibited growth of colo 201 cells transplanted in nude mice.
AB - The effect of conjugated docosahexaenoic acid (CDHA) on the inhibition of colon cancer cell growth was examined iyn the colo 20I human colon cancer cell line, and the effect was compared with docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA). CDHA was a more potent tumor cell growth inhibitor than DHA and EPA by colorimetric 3-(4,5-dimethylthiazol-2-yl)-5-(3y- carboxymethoxyphenyl)-2 -(4-sulfophenyl)-2H-tetrazolium (MTS) assay (IC 50for 72 h: 31.6 μM, 46.8 μM, and 56.6 μM, respectively). CDHA inhibited cell cycle progression, due to accumulation of cells in G1 phase, which involved increased p21Cip1/Waf1and decreased cyclin D1, cyclin E, and proliferating cell nuclear antigen expression; the p53 and cyclin A levels were unchanged. Induction of apoptosis was confirmed by the appearance of sub-G1 populations, and apoptosis cascade involved upregulation of the apoptosis-enhancing proteins (Bak and Bcl-xS) and downregulation of the apoptosis-suppressing proteins (Bcl-xL and Bcl-2). CDHA modulated cell cycle regulatory proteins and apoptosis-related proteins, similar to the effects of DHA. CDHA at a dietary dose of 1.0% significantly inhibited growth of colo 201 cells transplanted in nude mice.
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U2 - 10.1207/s15327914nc5001_10
DO - 10.1207/s15327914nc5001_10
M3 - Article
C2 - 15572300
AN - SCOPUS:9744230664
SN - 0163-5581
VL - 50
SP - 71
EP - 79
JO - Nutrition and Cancer
JF - Nutrition and Cancer
IS - 1
ER -
