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https://ir.cnu.edu.tw/handle/310902800/31019
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| 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
fluoxetine
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 |
| 顯示於類別: | [藥學系(所)] 期刊論文
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