Calycosin Induces Gastric Cancer Cell Apoptosis via the ROS-Mediated MAPK/STAT3/NF-κB Pathway

Yu Zhang1, Jian-Qiang Zhang2,3, Tong Zhang1

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

Abstract

Insights

Calycosin, a plant compound, effectively induces apoptosis and inhibits gastric cancer cell growth by increasing reactive oxygen species (ROS). This natural compound also impacts cell cycle progression and migration, offering potential anti-cancer benefits.

Area of Science:

  • Oncology
  • Pharmacology
  • Cell Biology

Background:

  • Calycosin, a plant-derived compound, exhibits anti-cancer properties by inducing apoptosis in various cancer cells.
  • The precise mechanism by which calycosin regulates reactive oxygen species (ROS) in gastric cancer (GC) remains incompletely understood.

Purpose of the Study:

  • To investigate the effects of calycosin on apoptosis, cell cycle, and migration in gastric cancer cells.
  • To elucidate the role of ROS regulation in calycosin's anti-cancer mechanisms.

Main Methods:

  • Cell Counting Kit-8 assay for cytotoxicity.
  • Hoechst 33342/propidium iodide staining and flow cytometry for apoptosis analysis.
  • Western blotting to assess protein expression (e.g., Bcl-2 family, caspases, signaling pathways).
  • Assessment of ROS levels and cell cycle/migration inhibition assays with n-acetyl-l-cysteine (NAC).

Main Results:

  • Calycosin demonstrated significant cytotoxicity against 12 gastric cancer cell lines, with no impact on normal cells.
  • Calycosin induced apoptosis in AGS cells, evidenced by increased pro-apoptotic markers (cytochrome C, Bad, cleaved caspase-3, cleaved PARP) and decreased anti-apoptotic Bcl-2.
  • Calycosin modulated signaling pathways (MAPK, STAT3, NF-κB), increased ROS accumulation, arrested cells in G0/G1 phase, and inhibited cell migration, effects reversed by NAC.

Conclusions:

  • Calycosin induces apoptosis in gastric cancer cells through ROS-mediated activation of MAPK/STAT3/NF-κB pathways.
  • Calycosin exerts anti-carcinogenic effects by regulating apoptosis, cell cycle, and migration in gastric cancer.
  • ROS generation is a critical mediator of calycosin's anti-cancer activity in gastric cancer cells.

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