Abstract
Background/Aim: The aim of present study was to verify the effect of fluoxetine on DNA repair and metastatic potential in non-small cell lung cancer (NSCLC) in vitro. Materials and Methods: Highly metastatic NSCLC CL1-5-F4 cells were used in this study. Cells were treated with different concentrations of fluoxetine or QNZ (NF-ĸB inhibitor) for 48 h. After treatment, cell viability, apoptotic signaling, NF-ĸB activation, expression of DNA repair and metastasis-associated proteins, and cell migration/invasion were evaluated by (4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium assay, flow cytometry, NF-ĸB reporter gene, western blotting, and cell migration/invasion assay, respectively. Results: Fluoxetine induced apoptosis and reduced cell viability, NF-ĸB activation, expression of DNA repair and metastasis-associated proteins, and cell migration/invasion in CL1-5-F4 cells. Also, NF-ĸB activation was the critical factor in fluoxetine-inhibited metastatic potential. Conclusion: Fluoxetine induced apoptosis and inhibited DNA repair and metastatic potential in NSCLC CL1-5-F4 cells.
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Wu, J. Y., Lin, S. S., Hsu, F. T., & Chung, J. G. (2018). Fluoxetine inhibits DNA repair and NF-ĸB-modulated metastatic potential in non-small cell lung cancer. Anticancer Research, 38(9), 5201–5210. https://doi.org/10.21873/anticanres.12843
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