Journal
MOLECULAR MEDICINE REPORTS
Volume 11, Issue 6, Pages 4694-4700Publisher
SPANDIDOS PUBL LTD
DOI: 10.3892/mmr.2015.3331
Keywords
esophageal cancer; non-steroidal anti-inflammatory drugs; Smac; indomethacin; apoptosis
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Funding
- Shannxi Province Science and Technology Fund [2010K01-133]
- Chinese National Natural Science Foundation [81272418, 81402506]
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The use of non-steroidal anti-inflammatory drugs (NSAIDs) has been associated with a reduced risk of various types of cancer, including esophageal cancer. However, the mechanisms underlying the antineoplastic effects of NSAIDs in esophageal cancer remain to be elucidated. In the present study, a significant inhibition in cell viability was observed in the EC109 cells following treatment with different concentrations of indomethacin, and these effects occurred in a dose- and time-dependent manner. This inhibition was due to the release of second mitochondria-derived activator of caspase (Smac) into the cytosol and the activation of caspase-3. Subsequently, flow cytometry was performed to investigate indomethacin-induced apoptosis following the overexpression or knockdown of Smac, and western blot analysis was performed to determine the expression of Smac and the activation of caspase-3. Overexpression of Smac was promoted apoptosis, while downregulation of Smac significantly inhibited apoptosis. Western blot analysis demonstrated that indomethacin induced apoptosis through releasing Smac into the cytosol and activating caspase-3. These results indicated that Smac is essential for the apoptosis induced by indomethacin in esophageal cancer cells.
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