Indomethacin induces apoptosis in the EC109 esophageal cancer cell line by releasing second mitochondria-derived activator of caspase and activating caspase-3

Sida Qin, Chongwen Xu, Shuo Li, Chengcheng Yang, Xin Sun, Xifang Wang, Shou Ching Tang, Hong Ren

Research output: Contribution to journalArticle

5 Scopus citations

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 languageEnglish (US)
Pages (from-to)4694-4700
Number of pages7
JournalMolecular Medicine Reports
Volume11
Issue number6
DOIs
StatePublished - 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

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