Gallic Acid Induces Apoptosis in Human Gastric Adenocarcinoma Cells

Anticancer Res. 2018 Apr;38(4):2057-2067. doi: 10.21873/anticanres.12445.


Background/aim: Gastric cancer is one of the most common malignant cancers with a poor prognosis and high mortality rate worldwide. Current treatment of gastric cancer includes surgery and chemotherapy as the main modalities, but the potentially severe side-effects of chemotherapy present a considerable challenge. Gallic acid is a trihydroxybenzoic acid found to exert an anticancer effect against a variety of cancer cells. The purpose of this study was to determine the anti-cancer activity of Galla chinensis and its main component gallic acid on human gastric adenocarcinoma cells.

Materials and methods: MTT assay and cell death ELISA were used to determine the apoptotic effect of Gallic Chinensis and gallic acid on human gastric adenocarcinoma cells. To determine the pathway and relevant components by which gallic acid-induced apoptosis is mediated through, cells were transfected with siRNA (Fas, FasL, DR5, p53) using Lipofectamine 2000. Reults: Gallic Chinensis and gallic acid induced apoptosis of human gastric adenocarcinoma cells. Gallic acid induced up-regulation of Fas, FasL, and DR5 expression in AGS cells. Transfection of cells with Fas, FasL, or DR5 siRNA reduced gallic acid-induced cell death. In addition, p53 was shown to be involved in gallic acid-mediated Fas, FasL, and DR5 expression as well as cell apoptosis in AGS cells.

Conclusion: These results suggest that gallic acid has a potential role in the treatment of gastric cancer.

Keywords: Gastric cancer; apoptosis; cytochrome c; gallic acid; human gastric adenocarcinoma cell line.

MeSH terms

  • Adenocarcinoma / genetics
  • Adenocarcinoma / metabolism
  • Adenocarcinoma / pathology*
  • Apoptosis / drug effects*
  • Cell Line, Tumor
  • Fas Ligand Protein / genetics
  • Fas Ligand Protein / metabolism
  • Gallic Acid / pharmacology*
  • Humans
  • Receptors, TNF-Related Apoptosis-Inducing Ligand / genetics
  • Receptors, TNF-Related Apoptosis-Inducing Ligand / metabolism
  • Signal Transduction / drug effects
  • Signal Transduction / genetics
  • Stomach Neoplasms / genetics
  • Stomach Neoplasms / metabolism
  • Stomach Neoplasms / pathology*
  • Up-Regulation / drug effects
  • fas Receptor / genetics
  • fas Receptor / metabolism


  • FASLG protein, human
  • Fas Ligand Protein
  • Receptors, TNF-Related Apoptosis-Inducing Ligand
  • TNFRSF10B protein, human
  • fas Receptor
  • Gallic Acid