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    Please use this identifier to cite or link to this item: https://ir.cnu.edu.tw/handle/310902800/34669

    標題: Auranofin induces urothelial carcinoma cell death via reactive oxygen species production and synergy with cisplatin
    作者: Chen, San-Yuan
    Chao, Chun-Nun
    Huang, Hsin-Yi
    Fang, Chiung-Yao
    貢獻者: Chia-Yi Christian Hospital
    Department of Sports Management, Chia Nan University of Pharmacy & Science
    Chia-Yi Christian Hospital
    Asia University Taiwan
    Chia-Yi Christian Hospital
    關鍵字: bladder-cancer
    anticancer activity
    日期: 2022
    上傳時間: 2023-12-11 14:04:06 (UTC+8)
    摘要: Urothelial carcinoma (UC) is one of the most common cancer types of the urinary tract. UC is associated with poor 5-year survival rate, and resistance to cisplatin-based therapy remains a challenge for invasive bladder cancer treatment. Therefore, there is an urgent need to develop new drugs for advanced UC therapy. Auranofin (AF) was developed over 30 years ago for the treatment of rheumatoid arthritis and has been reported to exert an antitumor effect by increasing the level of reactive oxygen species (ROS) in cancer cells. The aim of the present study was to examine the effects of AF on cancer cell proliferation, cell cycle and apoptosis, either alone or in combination with cisplatin. AF induced cell death in two separate cell lines, HT 1376 and BFTC 909, in a concentration- and time-dependent manner by inducing cell cycle arrest. However, the distribution of cells in different phases of the cell cycle differed between the two cell lines, with G(0)/G(1) cell cycle arrest in HT 1376 cells and S phase arrest in BFTC 909 cells. In addition, AF induced apoptosis in HT 1376, as well as redox imbalance in both HT 1376 and BFTC 909 cells. Cell viability was rescued following treatment with N-acetyl-L-cysteine, a ROS scavenger. Furthermore, AF treatment synergistically increased the cytotoxicity of HT 1376 and BFTC 909 cells when combined with cisplatin treatment. These findings suggest that AF may represent a potential candidate drug against UC and increase the therapeutic effect of cisplatin.
    關聯: ONCOLOGY LETTERS, v.23, n.2, pp.61
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