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https://ir.cnu.edu.tw/handle/310902800/30957
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| 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. |
| 關聯: | Food and Chemical Toxicology, v.97, pp.336-345 |
| 顯示於類別: | [休閒保健管理系(所)] 期刊論文
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