Author(s): Yang, JS (Yang, Jai-Sing); Chen, GW (Chen, Guang-Wei); Hsia, TC (Hsia, Te- Chun); Ho, HC (Ho, Heng-Chien); Ho, CC (Ho, Chin-Chin); Lin, MW (Lin, Meng-Wei); Lin, SS (Lin, Song-Shei); Yeh, RD (Yeh, Ru-Duan); Ip, SW (Ip, Siu-Wan); Lu, HF (Lu, Hsu-Fung);
Chung, JG (Chung, Jing-Gung)
Title: Diallyl disulfide induces apoptosis in human colon cancer cell line (COLO 205) through the induction of reactive oxygen species, endoplasmic reticulum stress, caspases casade and mitochondrial-dependent pathways
Source: FOOD AND CHEMICAL TOXICOLOGY, 47 (1): 171-179 JAN 2009 Language: English
Document Type: Article
Author Keywords: Diallyl disulfide; Caspase-3; Apoptosis; Mitochondria; Reactive oxygen species; cDNA microarray
KeyWords Plus: DNA-DAMAGE; CARCINOMA; DEATH; KINASE; GROWTH; CYCLE;
CYTOTOXICITY; ACTIVATION; INHIBITORS; EXPRESSION
Abstract: In this study, we investigated the effects of DADS on human colon cancer cell line COLO 205 on cell cycle arrest and apoptosis in vitro. After 24 h treatment of COLO 205 cells with DADS, the dose- and time-dependent decreases of viable cells were observed and the IC50 was 22.47 mu M. The decreased percentages of viable cells are associated with the production of ROS. Treatment of COLO 205 cells with DADS resulted in G2/M phase arrest and apoptosis occurrence through the mitochondrial-pathway (Bcl-2, Bcl-xL down-regulation and Bak, Bax up-regulation). DADS increased cyclin B, cdc25c-ser-216-9 and Weel but did not affect CDK1 protein and gene expression within 24 h of treatment. DADS-induced apoptosis was examined and confirmed by DAPI staining and DNA fragmentation assay.
DADS promoted caspase-3, -8 and -9 activity and induced apoptosis were accompanied by increasing the levels of Fas, phospho-Ask1 and JNK, p53 and decreasing the mitochondrial membrane potential which then led to release the cytochrome c, cleavage of pro-caspase-9 and -3. The COLO 205 cells were pre-treated with JNK inhibitor before leading to decrease the percentage of apoptosis which was induced by DADS. Inhibition of caspase-3 activation blocked DADS-induced apoptosis on COLO 205 cells. (C) 2008 Elsevier Ltd. All rights reserved.
Addresses: [Chung, Jing-Gung] China Med Univ, Dept Biol Sci & Technol, Taichung 404, Taiwan; [Yang, Jai-Sing; Lin, Meng-Wei] China Med Univ, Dept Pharmacol, Taichung 404, Taiwan; [Chen, Guang-Wei] Kaohsiung Med Univ, Chung Ho Mem Hosp, Dept Tradit Chinese Med, Kaohsiung 807, Taiwan; [Hsia, Te-Chun] China Med Univ Hosp, Dept Internal Med, Taichung 404, Taiwan; [Ho, Heng-Chien] China Med Univ, Dept Biochem, Taichung 404, Taiwan; [Ho, Chin-Chin] Cent Taiwan Univ Sci & Technol, Dept Nurse, Taichung 406, Taiwan;
[Lin, Song-Shei] Cent Taiwan Univ Sci & Technol, Dept Radiol Technol, Taichung 406,
Taiwan; [Yeh, Ru-Duan] Chung Shan Med Univ Hosp, Dept Integrated Chinese Western Med, Taichung 402, Taiwan; [Ip, Siu-Wan] China Med Univ, Dept Nutr, Taichung 404, Taiwan; [Lu, Hsu-Fung] Cheng Hsin Rehabil Med Ctr, Dept Clin Pathol, Taipei 112, Taiwan; [Chung, Jing- Gung] Asia Univ, Dept Biotechnol, Wufeng 413, Taichung County, Taiwan
Reprint Address: Chung, JG, China Med Univ, Dept Biol Sci & Technol, 91 Hsueh Shih Rd, Taichung 404, Taiwan.
E-mail Address: [email protected] Funding Acknowledgement:
Funding Agency Grant Number
NSC 91-2320-B-039-028
92-2320-B-039-034 National Science Council of Taiwan
This work was supported by Grant NSC 91-2320-B-039-028 and NSC 92-2320-B-039-034 from National Science Council of Taiwan.
Cited References: ALNEMRI ES, 1996, CELL, V87, P171.
BUIATTI E, 1989, INT J CANCER, V44, P611.
CASTEDO M, 2002, CELL DEATH DIFFER, V9, P1287, DOI 10.1038/sj.cdd.4401130.
CHEN YC, 1996, MOL CARCINOGEN, V17, P224.
CHUNG JG, 2001, CANCER RES, V61, P8873.
CHUNG JG, 2007, PROTEOMICS, V7, P3305, DOI 10.1002/pmic.200700200.
FADEEL B, 1999, BIOCHEM BIOPH RES CO, V266, P699.
FERREIRA CG, 2002, CLIN CANCER RES, V8, P2024.
FILOMENI G, 2003, CANCER RES, V63, P5940.
HAENSZEL W, 1972, J NATL CANCER I, V49, P969.
HONG YS, 2000, EXP MOL MED, V32, P127.
HSU SC, 2007, ANTICANCER RES, V27, P2415.
JACKSON JR, 2000, CANCER RES, V60, P566.
JACOBSON MD, 1997, CELL, V88, P347.
KALBACOVA M, 2003, CYTOM PART A A, V52, P110, DOI 10.1002/cyto.a.10031.
KING RW, 1994, CELL, V79, P563.
KWON KB, 2002, BIOCHEM PHARMACOL, V63, P41.
LEE YM, 2003, TOXICOL IN VITRO, V17, P279, DOI 10.1016/S0887-2333(03)00014-6.
LIAO QJ, 2007, AI ZHENG, V26, P828.
LIUZZI F, 2003, ANN NY ACAD SCI, V1010, P441, DOI 10.1196/annals.1299.080.
LU HF, 2004, FOOD CHEM TOXICOL, V42, P1543, DOI 10.1016/j.fct.2003.06.001.
MCGOWAN CH, 1993, EMBO J, V12, P75.
NAKAGAWA H, 2001, CARCINOGENESIS, V22, P891.
OOI BS, 2001, ANZ J SURG, V71, P703.
PARK EK, 2002, EXP MOL MED, V34, P250.
PETTIT GR, 1996, J ETHNOPHARMACOL, V53, P57.
RUVOLO PP, 2001, LEUKEMIA, V15, P515.
SLEE EA, 1999, J CELL BIOL, V144, P281.
SUNDARAM SG, 1996, CARCINOGENESIS, V17, P669.
TAKAHASHI S, 1992, CARCINOGENESIS, V13, P1513.
WANG SC, 2006, MUTAT RES-FUND MOL M, V593, P9, DOI 10.1016/j.mrfmmm.2005.06.023.
WEN J, 2004, BIOCHEM PHARMACOL, V68, P323, DOI 10.1016/j.bcp.2004.03.027.
XIANG SL, 2005, AI ZHENG, V24, P940.
YANG SH, 2007, LEUKEMIA RES, V31, P1413, DOI 10.1016/j.leukres.2007.02.014.
YU SW, 2002, SCIENCE, V297, P259.
ZHAO J, 2006, ACTA PHARMACOL SIN, V27, P1459, DOI 10.1111/j.1745- 7254.2006.00433.x.
Cited Reference Count: 36 Times Cited: 8
Publisher: PERGAMON-ELSEVIER SCIENCE LTD
Publisher Address: THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
ISSN: 0278-6915
DOI: 10.1016/j.fct.2008.10.032
29-char Source Abbrev.: FOOD CHEM TOXICOL ISO Source Abbrev.: Food Chem. Toxicol.
Source Item Page Count: 9
Subject Category: Food Science & Technology; Toxicology ISI Document Delivery No.: 399BR
