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    Please use this identifier to cite or link to this item: http://asiair.asia.edu.tw/ir/handle/310904400/108293


    Title: Dithiothreitol Enhanced Arsenic-Trioxide-Induced Cell Apoptosis in Cultured Oral Cancer Cells via Mitochondrial Dysfunction and Endoplasmic Reticulum Stress
    Authors: Bau, 蔡佳紋;Chia-Wen Tsai;Mei-Due Yang;Mei-Due Yang;Te-Chun Hsia;Te-Chun Hsia;Wen-Shin Cha;Wen-Shin Chang;Chin-Mu Hsu;Chin-Mu Hsu;Yi-Hsien Hsi;Yi-Hsien Hsieh;Jing-Gung Ch;Jing-Gung Chung;包大?;Da-Tian
    Contributors: 生物資訊與醫學工程學系
    Date: 2017-01
    Issue Date: 2017-11-03 06:07:26 (UTC+0)
    Abstract: Arsenic is naturally occurring toxic metalloid and drinking As2O3 containing water are recognized to be related to increased risk of neurotoxicity, liver injury, blackfoot disease, hypertension, and cancer. On the contrary, As2O3 has been an ancient drug used in traditional Chinese medicine with substantial anticancer activities, especially in the treatment of acute promyelocytic leukemia as well as chronic wound healing. However, the cytotoxicity and detail mechanisms of As2O3 action in solid cancer cells, such as oral cancer cells, are largely unknown. In this study, we have primarily cultured four pairs of tumor and nontumor cells from the oral cancer patients and treated the cells with As2O3 alone or combined with dithiothreitol (DTT). The results showed that 0.5 μM As2O3 plus 20 μM DTT caused a significant cell death of oral cancer cells but not the nontumor cells. Also As2O3 plus DTT upregulated Bax and Bak, downregulated Bcl-2 and p53, caused a loss of mitochondria membrane potential in oral cancer cells. On the other way, As2O3 also triggered endoplasmic reticulum stress and increased the levels of glucose-regulated protein 78, calpain 1 and 2. Our results suggest that DTT could synergistically enhance the effects of As2O3 on killing oral cancer cells while nontoxic to the nontumor cells. The combination is promising for clinical practice in oral cancer therapy and worth further investigations. © 2015 Wiley Periodicals, Inc. Environ Toxicol 32: 17–27, 2017.
    Relation: ENVIRONMENTAL TOXICOLOGY
    Appears in Collections:[生物資訊與醫學工程學系 ] 期刊論文

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