Journal
ANTICANCER RESEARCH
Volume 39, Issue 11, Pages 6155-6163Publisher
INT INST ANTICANCER RESEARCH
DOI: 10.21873/anticanres.13823
Keywords
Gastric adenocarcinoma cells; apoptosis; necroptosis
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Funding
- Basic Science Research Program through the National Research Foundation of Korea (NRF) - Ministry of Education, Science and Technology [2016R1D1A1A09918019]
- National Research Foundation of Korea [2016R1D1A1A09918019] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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Background/Aim: Fluoxetine, an antidepressant, has cytotoxic effects on several cancer cell lines, while paclitaxel is an antineoplastic agent for various cancers. The aim of this study was to evaluate whether fluoxetine enhances the cytotoxic effect of paclitaxel in gastric adenocarcinoma cells and determine the mechanism of cell death. Materials and Methods: 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay was used to examine cell viability and perform cell cycle analysis. Annexin V propidium iodide (PI) staining, 4',6-diamidino-2-phenylindole ( DAPI) staining, caspase-3/7 assay, and western blot analysis were performed for determining cell death. Results: Fluoxetine enhanced the anti-proliferative effect of paclitaxel. Fluoxetine-paclitaxel combination caused G(2)/M arrest and increased events in the sub G(0)/G(1) phase in a time and dose-dependent manner, indicating apoptotic cell death. Combination treatment caused an increase in early apoptotic and late apoptotic cell death compared to single treatment alone. Conclusion: Fluoxetine enhanced the antiproliferation effect of paclitaxel in gastric adenocarcinoma AGS cells and the combination caused cell death by triggering apoptosis and necroptosis.
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