evp-4593 and Lung-Neoplasms

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.. 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.. 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.. Fluoxetine induced apoptosis and inhibited DNA repair and metastatic potential in NSCLC CL1-5-F4 cells.

Topics: Carcinoma, Non-Small-Cell Lung; Cell Line, Tumor; Cell Movement; Cell Proliferation; Cell Survival; DNA Repair; Fluoxetine; Gene Expression Regulation, Neoplastic; Humans; Lung Neoplasms; Neoplasm Metastasis; NF-kappa B; Phenyl Ethers; Quinazolines; Signal Transduction