Induction of apoptosis by eicosapentaenoic acid in esophageal squamous cell carcinoma

Anticancer Res. 2014 Dec;34(12):7145-9.

Abstract

Background: Eicosapentaenoic acid (EPA) suppresses the proliferation of cell lines derived from colon, pancreatic, breast and other cancers. Few reports have described the effect of EPA on esophageal cancer cell lines.

Materials and methods: We investigated the effect of EPA on the proliferation of the esophageal squamous cell carcinoma cell lines TE11 and KYSE180 with a WST-1 assay. Apoptosis was evaluated with a DNA fragmentation assay. Levels of apoptosis-related proteins (caspase-3, -7, -9 and poly (ADP-ribose) polymerase (PARP)) and cleaved caspase-3, -7, -9 and PARP were evaluated by western blot analysis.

Results: After exposure to EPA for 24 h, KYSE180 and TE11 cell proliferation was suppressed in a dose-dependent manner (p<0.05). In addition, caspase -3, -7, -9 and PARP were activated. EPA (0.1 μM, 1 μM, 10 μM) induced apoptosis in a dose-dependent manner, as detected by the DNA fragmentation assay.

Conclusion: EPA shows potential as a new treatment for esophageal cancer.

Keywords: Eicosapentaenoic acid; apoptosis; esophageal cancer.

MeSH terms

  • Antineoplastic Agents / pharmacology*
  • Apoptosis / drug effects*
  • Carcinoma, Squamous Cell / pathology*
  • Caspase 3 / biosynthesis
  • Caspase 3 / metabolism
  • Caspase 7 / biosynthesis
  • Caspase 7 / metabolism
  • Caspase 9 / biosynthesis
  • Caspase 9 / metabolism
  • Cell Line, Tumor
  • Cell Proliferation / drug effects
  • DNA Fragmentation / drug effects
  • Eicosapentaenoic Acid / pharmacology*
  • Esophageal Neoplasms / pathology*
  • Esophageal Squamous Cell Carcinoma
  • Humans
  • Poly(ADP-ribose) Polymerases / biosynthesis
  • Poly(ADP-ribose) Polymerases / metabolism

Substances

  • Antineoplastic Agents
  • Eicosapentaenoic Acid
  • Poly(ADP-ribose) Polymerases
  • Caspase 3
  • Caspase 7
  • Caspase 9