Chia Nan University of Pharmacy & Science Institutional Repository:Item 310902800/28501
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    標題: An Increase in Reactive Oxygen Species by Deregulation of ARNT Enhances Chemotherapeutic Drug-Induced Cancer Cell Death
    作者: Shieh, Jiunn-Min
    Shen, Chih-Jie
    Chang, Wei-Chiao
    Cheng, Hung-Chi
    Chan, Ya-Yi
    Huang, Wan-Chen
    Chang, Wen-Chang
    Chen, Ben-Kuen
    貢獻者: 通識教育中心
    關鍵字: RECEPTOR NUCLEAR TRANSLOCATOR
    TRANSCRIPTION FACTOR
    GENE-EXPRESSION
    APOPTOSIS
    ACTIVATION
    STRESS
    AHR
    DOXORUBICIN
    RESPONSES
    MDR1
    日期: 2014-06
    上傳時間: 2015-05-06 21:18:33 (UTC+8)
    出版者: Public Library Science
    摘要: Background: Unique characteristics of tumor microenvironments can be used as targets of cancer therapy. The aryl hydrocarbon receptor nuclear translocator (ARNT) is an important mediator of tumor progression. However, the functional role of ARNT in chemotherapeutic drug-treated cancer remains unclear. Methodology/Principal Findings: Here, we found that knockdown of ARNT in cancer cells reduced the proliferation rate and the transformation ability of those cells. Moreover, cisplatin-induced cell apoptosis was enhanced in ARNT-deficient cells. Expression of ARNT also decreased in the presence of cisplatin through proteasomal degradation pathway. However, ARNT level was maintained in cisplatin-treated drug-resistant cells, which prevented cell from apoptosis. Interestingly, reactive oxygen species (ROS) dramatically increased when ARNT was knocked down in cancer cells, enhancing cisplatin-induced apoptosis. ROS promoted cell death was inhibited in cells treated with the ROS scavenger, N-acetyl-cysteine (NAC). Conclusions/Significance: These results suggested that the anticancer activity of cisplatin is attributable to its induction of the production of ROS by ARNT degradation. Targeting ARNT could be a potential strategy to eliminate drug resistance in cancer cells.
    關聯: Plos One, v.9 n.6, e99242
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