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Jaceosidin induces apoptosis and inhibits migration in AGS gastric cancer cells by regulating ROS-mediated signaling

Jian Liu1, Shu-Mei Li2, Yan-Jun Tang3

  • 1College of Life Science and Technology, Heilongjiang Bayi Agricultural University, Daqing, People's Republic of China.

Redox Report : Communications in Free Radical Research
|February 6, 2024
PubMed

Insights

Jaceosidin (JAC), a natural flavonoid, effectively combats gastric cancer by inducing apoptosis and cell cycle arrest. Its anti-cancer effects are mediated by reactive oxygen species (ROS) signaling pathways.

Area of Science:

  • Natural Product Chemistry
  • Molecular Pharmacology
  • Cancer Biology

Background:

  • Jaceosidin (JAC) is a natural flavonoid with known antioxidant properties.
  • The precise anti-cancer mechanism of JAC, particularly in gastric cancer, requires elucidation.

Purpose of the Study:

  • To investigate the anti-cancer mechanism of Jaceosidin (JAC) in human gastric adenocarcinoma AGS cells.
  • To identify the key signaling pathways involved in JAC's cytotoxic and anti-proliferative effects.

Main Methods:

  • Cytotoxicity and apoptosis assays were performed.
  • Network pharmacology analysis was employed to predict signaling pathways.
  • Western blotting was used to analyze protein expression changes.
  • Cell cycle and migration assays were conducted.

Main Results:

  • JAC induced apoptosis in AGS cells via the mitochondrial pathway.
  • JAC modulated reactive oxygen species (ROS) levels, impacting AKT and MAPK signaling.
  • JAC caused G0/G1 phase arrest by regulating cell cycle proteins and inhibited cell migration by affecting the Wnt/β-catenin pathway.
  • N-acetyl cysteine reversed these protein expression changes, confirming ROS mediation.

Conclusions:

  • Jaceosidin (JAC) exhibits anti-cancer properties against gastric cancer cells.
  • JAC exerts its effects through ROS-mediated induction of apoptosis, G0/G1 cell cycle arrest, and inhibition of migration.
Keywords:
Jaceosidincell apoptosiscell cyclecell migrationcytotoxicitygastric cancernetwork pharmacologyreactive oxygen species

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