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    CMUR > College of Medicine > School of Medicine > Journal articles >  Item 310903500/30837
    Please use this identifier to cite or link to this item: http://ir.cmu.edu.tw/ir/handle/310903500/30837


    Title: Diallyl disulfide inhibits N-acetyltransferase activity and gene expression in human esophagus epidermoid carcinoma CE 81T/VGH cells
    Authors: Yu, FS;Yu, CS;Lin, JP;Chen, SC;Lai, WW;Chung, JG
    Contributors: 醫學院醫學系微生物學科;China Med Univ, Dept Microbiol, Taichung, Taiwan;China Med Univ, Sch Dent, Taichung, Taiwan;China Med Univ, Ctr Gen Educ, Taichung, Taiwan;China Med Univ, Inst Chinese Med Sci, Taichung, Taiwan;Natl Kaohsiung Normal Univ, Dept Biotechnol, Kaohsiung, Taiwan;Hung Kuang Univ, Dept Food & Nutr, Taichung, Taiwan
    Date: 2005
    Issue Date: 2010-09-24 15:02:56 (UTC+8)
    Publisher: PERGAMON-ELSEVIER SCIENCE LTD
    Abstract: The mechanisms involved in the apoptotic effect of LCY-2-CHO [9-(2-chlorobenzyl)-9H-carbazole-3-carbaldehyde], a synthetic carbazole derivative identified as an anti-inflammatory compound, were studied. Cell cycle analysis by propidium iodide staining in human THP-1 monocytic leukemia cells showed the ability of LCY-2-CHO to increase cell population in sub-G1 stage with time- and concentration-dependent manners. LCY-2-CHO-mediated cell death was also demonstrated by DNA laddering and was not related to the release of lactate dehydrogenase. Apoptosis in THP-1 cells induced by LCY-2-CHO was accompanied by the Bid cleavage, collapse of mitochondrial transmembrane potential, the release of cytochrome c and the activation of caspase-3. The apoptotic effect of LCY-2-CHO was diminished by the presence of zVEID-fmk (caspase-6 inhibitor), zIETD-fmk (caspase-8 inhibitor), and zVAD-fmk (non-selective caspase inhibitor), but was not altered by several antioxidants, and cathepsin inhibitor. The Bid cleavage and loss of mitochondrial transmembrane potential, but not the cytochrome c release, were reversed by zIETD-fmk. Comparing the cell selectivity of LCY-2-CHO, we found T-cell acute lymphoblastic CEM leukemia cells were sensitive to 1 mu M LCY-2-CHO, acute myeloid leukemia HL-60 cells underwent apoptosis at 10 mu M, while adherent cancer cells, such as PC3, HT29 and MCF-7, were resistant to 30 mu M LCY-2-CHO within 24-h incubation. Taken together in the present study, we demonstrated LCY-2-CHO might be apoptotic for malignant hematopoietic cells but not anchorage-dependent cells. This action is mediated by an intrinsic caspase-dependent apoptotic event involving mitochondria. (c) 2005 Elsevier Inc. All rights reserved.
    Relation: FOOD AND CHEMICAL TOXICOLOGY 43(7):1029-1036
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