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 |
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| Authors: | Jai-Sing Yang Guang-Wei Chen Te-Chun Hsia Heng-Chien Ho Chin-Chin Ho Meng-Wei Lin Song-Shei Lin Ru-Duan Yeh Siu-Wan Ip Hsu-Fung Lu Jing-Gung Chung |
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| Affiliation: | 1. Department of Pharmacology, China Medical University, Taichung 404, Taiwan;2. Department of Traditional Chinese Medical, Chung-Ho Memorial Hospital, Kaohsiung Medical University, Kaohsiung 807, Taiwan;3. Department of Internal Medicine, China Medical University Hospital, Taichung 404, Taiwan;4. Department of Biochemistry, China Medical University, Taichung 404, Taiwan;5. Department of Nurse, Central Taiwan University of Science and Technology, Beitun District, Taichung 406, Taiwan;6. Department of Radiological Technology, Central Taiwan University of Science and Technology, Beitun District, Taichung 406, Taiwan;g Department of Integrated Chinese Western Medicine, Chung Shan Medical University Hospital, Taichung 402, Taiwan;h Department of Nutrition, China Medical University, Taichung 404, Taiwan;i Department of Clinical Pathology, Cheng Hsin Rehabilitation Medical Center, Taipei 112, Taiwan;j Department of Biological Science and Technology, China Medical University, 91 Hsueh-Shih Road, Taichung 404, Taiwan;k Department of Biotechnology, Asia University, Wufeng, Taichung County 413, Taiwan |
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| 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 μM. 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 Wee1 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. |
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| Keywords: | CDK, cyclin-dependent protein kinase DADS, diallyl disulfide ΔΨm, mitochondria membrane potential NAC, N-acetylcysteine PI, propidium iodide ROS, reactive oxygen species |
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