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    Please use this identifier to cite or link to this item: http://ir.cnu.edu.tw/handle/310902800/31019

    標題: Fluoxetine regulates cell growth inhibition of interferon-alpha
    作者: Lin, Yu-Min
    Yu, Bu-Chin
    Chiu, Wen-Tai
    Sun, Hung-Yu
    Chien, Yu-Chieh
    Su, Hui-Chen
    Yen, Shu-Yang
    Lai, Hsin-Wen
    Bai, Chyi-Huey
    Young, Kung-Chia
    Tsao, Chiung-Wen
    貢獻者: Shin Kong Wu Ho Su Mem Hosp, Dept Gastroenterol
    Fu Jen Catholic Univ, Sch Med
    Univ Tokyo, Grad Sch Agr & Life Sci, Dept Anim Resource Sci
    Univ Tokyo, Grad Sch Agr & Life Sci, Dept Appl Biol Chem
    Natl Cheng Kung Univ, Coll Engn, Dept Biomed Engn
    Natl Cheng Kung Univ, Coll Med, Dept Med Lab Sci & Biotechnol
    Chung Hwa Univ Med Technol, Dept Nursing
    Chi Mei Med Ctr, Dept Pharm
    Chia Nan Univ Pharm & Sci, Dept Pharm
    Taipei Med Univ, Coll Med, Dept Publ Hlth
    關鍵字: interferon-alpha
    growth inhibition
    signal transducer and transactivator-1
    peroxisome proliferator-activated receptor-alpha
    日期: 2016-10
    上傳時間: 2018-01-18 11:39:58 (UTC+8)
    出版者: Spandidos Publ Ltd
    摘要: Fluoxetine, a well-known anti-depression agent, may act as a chemosensitizer to assist and promote cancer therapy. However, how fluoxetine regulates cellular signaling to enhance cellular responses against tumor cell growth remains unclear. In the present study, addition of fluoxetine promoted growth inhibition of interferon-alpha (IFN-alpha) in human bladder carcinoma cells but not in normal uroepithelial cells through lessening the IFN-alpha-induced apoptosis but switching to cause G1 arrest, and maintaining the IFN-amediated reduction in G2/M phase. Activations and signal transducer and transactivator (STAT)-1 and peroxisome proliferator-activated receptor alpha (PPAR-alpha) were involved in this process. Chemical inhibitions of STAT-1 or PPAR-alpha partially rescued bladder carcinoma cells from IFN-amediated growth inhibition via blockades of G1 arrest, cyclin D1 reduction, p53 downregulation and p27 upregulation in the presence of fluoxetine. However, the functions of both proteins were not involved in the control of fluoxetine over apoptosis and maintained the declined G2/M phase of IFN-alpha. These results indicated that activation of PPAR-alpha and STAT-1 participated, at least in part, in growth inhibition of IFN-alpha in the presence of fluoxetine.
    關聯: International Journal of Oncology, v.49 n.4, pp.1746-1754
    Appears in Collections:[藥學系(所)] 期刊論文

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