Fluoxetine regulates cell growth inhibition of interferon-α

Yu Min Lin, Bu Chin Yu, Wen Tai Chiu, Hung Yu Sun, Yu Chieh Chien, Hui Chen Su, Shu Yang Yen, Hsin Wen Lai, Chyi Huey Bai, Kung Chia Young, Chiung Wen Tsao

Research output: Contribution to journalArticlepeer-review

8 Citations (Scopus)


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.

Original languageEnglish
Pages (from-to)1746-1754
Number of pages9
JournalInternational Journal of Oncology
Issue number4
Publication statusPublished - Oct 2016


  • Fluoxetine
  • Growth inhibition
  • Interferon-α
  • Peroxisome proliferator-activated receptor-α
  • Signal transducer and transactivator-1

ASJC Scopus subject areas

  • Oncology
  • Cancer Research


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