Fluoxetine regulates cell growth inhibition of interferon-alpha

doi:10.3892/ijo.2016.3650

Chia Nan University of Pharmacy & Science Institutional Repository > 藥理學院 > 藥學系(所) > 期刊論文 > Item 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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