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Isovanillin regulates gastric cancer cells apoptosis and metastasis by targeting ROS-mediated MAPK and PI3K signaling

Jing-Jing Wen1, Xiao-Yu Jin2, Ying-Hua Luo3

  • 1Department of Biochemistry and Molecular Biology, College of Life Science and Biotechnology, Heilongjiang Bayi Agricultural University.

Anti-Cancer Drugs
|January 17, 2026
PubMed

Insights

Isovanillin, a natural compound, effectively combats gastric cancer by inducing apoptosis and cell cycle arrest. It inhibits cancer cell migration by modulating reactive oxygen species (ROS) and key signaling pathways like PI3K/AKT and MAPK.

Area of Science:

  • Natural product chemistry
  • Molecular oncology
  • Pharmacology

Background:

  • Isovanillin is a natural coumarin with known biological activities.
  • Its specific mechanisms against gastric cancer remain largely unelucidated.
  • Understanding these pathways is crucial for developing novel anti-gastric cancer therapies.

Purpose of the Study:

  • To investigate the underlying molecular mechanisms of isovanillin's anti-gastric cancer effects.
  • To identify key signaling pathways and molecular targets involved in isovanillin's action.
  • To evaluate isovanillin's impact on gastric cancer cell viability, apoptosis, cell cycle, and metastasis.

Main Methods:

  • Network pharmacological analysis to identify potential targets.
  • Cell viability assays to assess isovanillin's effect on gastric cancer cell lines.
  • Apoptosis, cell cycle, and cell metastasis assays to evaluate functional outcomes.
  • Western blotting to analyze protein expression changes in key signaling pathways.
  • Reactive oxygen species (ROS) assays and scavenger experiments to determine ROS involvement.

Main Results:

  • Isovanillin significantly reduced gastric cancer cell viability.
  • Network pharmacology identified 41 key targets, implicating PI3K/AKT, MAPK, and ROS pathways.
  • Isovanillin promoted apoptosis, induced G2/M phase arrest, and suppressed cell migration.
  • These effects were mediated by ROS accumulation, influencing MAPK and PI3K/AKT signaling.
  • N-acetyl-l-cysteine reversed isovanillin-induced protein expression changes, confirming ROS mediation.

Conclusions:

  • Isovanillin exhibits potent anti-gastric cancer properties by inducing apoptosis and cell cycle arrest.
  • It inhibits gastric cancer cell migration through ROS-mediated regulation of MAPK and PI3K/AKT pathways.
  • Isovanillin represents a promising therapeutic candidate for gastric cancer treatment.
Keywords:
gastric cancerisovanillinmitogen-activated protein kinasephosphoinositide 3-kinasereactive oxygen species

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