Abstract
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.
Original language | English (US) |
---|---|
Pages (from-to) | 4694-4700 |
Number of pages | 7 |
Journal | Molecular Medicine Reports |
Volume | 11 |
Issue number | 6 |
DOIs | |
State | Published - Jun 1 2015 |
Keywords
- Apoptosis
- Esophageal cancer
- Indomethacin
- Non-steroidal anti-inflammatory drugs
- Smac
ASJC Scopus subject areas
- Biochemistry
- Molecular Medicine
- Molecular Biology
- Genetics
- Oncology
- Cancer Research