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    Please use this identifier to cite or link to this item: http://ir.cnu.edu.tw/handle/310902800/30957


    標題: Benzyl isothiocyanate promotes apoptosis of oral cancer cells via an acute redox stress-mediated DNA damage response
    作者: Yeh, Yao-Tsung
    Hsu, Yen-Nien
    Huang, Sheng-Yun
    Lin, Jian-Sheng
    Chen, Zi-Feng
    Chow, Nan-Haw
    Su, Shu-Hui
    Shyu, Huey-Wen
    Lin, Ching-Chiang
    Huang, Wu-Tein
    Yeh, Hua
    Chih, Yu-chia
    Huang, Yu-Hsuan
    Su, Shu-Jem
    貢獻者: Fooyin Univ, Sch Med & Hlth Sci, Dept Med Lab Sci & Biotechnol
    Fooyin Univ, Aging & Dis Prevent Res Ctr
    Fooyin Univ Hosp, Dept Educ & Res
    Yen Nien Biotechnol Co Ltd
    Natl Cheng Kung Univ, Coll Med, Dept Pathol
    Tzu Chi Univ, Coll Life Sci, Dept Mol Biol & Human Genet
    Fooyin Univ Hosp, Dept Lab Med
    Chia Nan Univ Pharm & Sci, Dept Recreat & Hlth Care Management
    關鍵字: Benzyl isothiocyanate
    Oral squamous cell carcinoma
    DNA damage
    Apoptosis
    Redox stress
    日期: 2016-11
    上傳時間: 2018-01-18 11:38:42 (UTC+8)
    出版者: Pergamon-Elsevier Science Ltd
    摘要: Benzyl isothiocyanate (BITC) is a cruciferous vegetable-derived compound with anticancer properties in human cancer cells. However, its anticancer potential and underlying mechanisms remain absent in human oral cancer cells. Results indicate that BITC inhibits growth, promotes G(2)/M phase arrest and triggers apoptosis of OC2 cells with a minimal toxicity to normal cells. BITC-induced cell death was completely prevented by pretreatment with thiol-containing redox compounds including N-acetyl-L-cysteine (NAC), glutathione (GSH), dithiothreitol, and 2-mercaptoethanol, but not free radical scavengers mito-TEMPO, catalase, apocynin, L-NAME and mannitol. BITC rapidly produced reactive oxygen species and nitric oxide, triggered oxidative DNA damage. BITC effectively decreased the intracellular GSH and GSH/GSSG ratio and redox balance recovery by thiol-containing redox compounds, but not by free radical scavengers. Accordingly, redox stresses-DNA damage response (DDR) activated ATM, Chk2, p53, and p21 and subsequently resulted in G(2)/M phase arrest by inhibiting Cdc2 and cyclin B1. Notably, BITC-induced apoptosis was associated with reduced Mcl-1 and Bcl-2 expression, diminished mitochondrial membrane potential (Delta Psi m), and increased PARP cleavage. These BITC-induced redox stress-mediated DDR and apoptosis could be blocked by NAC and GSH. Therefore, BITC can be a rational drug candidate for oral cancer and acted via a redox-dependent pathway. (C) 2016 Elsevier Ltd. All rights reserved.
    Appears in Collections:[休閒保健管理系(所)] 期刊論文

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