TY - JOUR
T1 - Fluoxetine inhibits DNA repair and NF-ĸB-modulated metastatic potential in non-small cell lung cancer
AU - Wu, Jeng Yuan
AU - Lin, Song Shei
AU - Hsu, Fei Ting
AU - Chung, Jing Gung
N1 - Publisher Copyright:
© 2018 International Institute of Anticancer Research. All rights reserved.
PY - 2018/9/1
Y1 - 2018/9/1
N2 - 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.
AB - 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.
KW - DNA repair
KW - Fluoxetine
KW - Metastatic potential
KW - NF-ĸB
KW - Non-small cell lung cancer
KW - DNA repair
KW - Fluoxetine
KW - Metastatic potential
KW - NF-ĸB
KW - Non-small cell lung cancer
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U2 - 10.21873/anticanres.12843
DO - 10.21873/anticanres.12843
M3 - Article
C2 - 30194168
AN - SCOPUS:85053006579
SN - 0250-7005
VL - 38
SP - 5201
EP - 5210
JO - Anticancer Research
JF - Anticancer Research
IS - 9
ER -
