Fluoxetine regulates cell growth inhibition of interferon-α
| Autor: | Kung Chia Young, Chiung Wen Tsao, Shu Yang Yen, Yu Chieh Chien, Hui Chen Su, Hung Yu Sun, Hsin Wen Lai, Yu Min Lin, Bu Chin Yu, Wen Tai Chiu, Chyi Huey Bai |
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| Rok vydání: | 2016 |
| Předmět: |
0301 basic medicine
Cancer Research Blotting Western Chemosensitizer Biology Antiviral Agents 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Cyclin D1 Downregulation and upregulation Fluoxetine Tumor Cells Cultured Humans Fluorescent Antibody Technique Indirect Cell Proliferation Cell growth Interferon-alpha Cell cycle Flow Cytometry 030104 developmental biology Urinary Bladder Neoplasms Oncology chemistry Apoptosis 030220 oncology & carcinogenesis Cancer research Peroxisome proliferator-activated receptor alpha Growth inhibition Selective Serotonin Reuptake Inhibitors Signal Transduction |
| Zdroj: | International Journal of Oncology. 49:1746-1754 |
| ISSN: | 1791-2423 1019-6439 |
| DOI: | 10.3892/ijo.2016.3650 |
| Popis: | 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-α) in human bladder carcinoma cells but not in normal uroepithelial cells through lessening the IFN-α-induced apoptosis but switching to cause G1 arrest, and maintaining the IFN-α-mediated reduction in G2/M phase. Activations and signal transducer and transactivator (STAT)-1 and peroxisome proliferator-activated receptor alpha (PPAR-α) were involved in this process. Chemical inhibitions of STAT-1 or PPAR-α partially rescued bladder carcinoma cells from IFN-α-mediated 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-α. These results indicated that activation of PPAR-α and STAT-1 participated, at least in part, in growth inhibition of IFN-α in the presence of fluoxetine. |
| Databáze: | OpenAIRE |
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