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Vitexin Inhibits Gastric Cancer Growth and Metastasis through HMGB1-mediated Inactivation of the PI3K/AKT/mTOR/HIF-1α

Peng Zhou1,2, Zi-Han Zheng2, Tao Wan2

  • 1Department of General Surgery, First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, People's Republic of China.

Journal of Gastric Cancer
|January 26, 2022
PubMed
Abstract

Insights

The flavonoid vitexin shows therapeutic potential against gastric cancer (GC) by inhibiting cell viability, migration, and invasion. Vitexin suppresses the HMGB1-mediated PI3K/Akt/HIF-1α pathway, offering a promising treatment for GC.

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Gastric cancer (GC) presents significant global health challenges due to high morbidity and mortality.
  • Flavonoids, like vitexin, possess known anti-tumor properties warranting investigation.
  • Understanding the molecular mechanisms of potential GC therapeutics is crucial.

Purpose of the Study:

  • To investigate the therapeutic potential of vitexin in gastric cancer.
  • To elucidate the underlying molecular mechanisms of vitexin's action in GC.

Main Methods:

  • Cell viability, migration, and invasion assays (MTT, scratch wound healing, transwell).
  • Western blotting for target molecule expression.
  • In vivo studies in nude mice for tumor growth and metastasis, with immunohistochemistry analysis.

Main Results:

  • Vitexin dose-dependently inhibited GC cell viability, migration, invasion, and epithelial-mesenchymal transition (EMT).
  • Vitexin inactivated the PI3K/AKT/HIF-1α pathway by repressing HMGB1 expression.
  • Vitexin suppressed xenograft tumor growth and liver metastasis in vivo by inhibiting HMGB1 expression.

Conclusions:

  • Vitexin inhibits gastric cancer progression by suppressing HMGB1-mediated PI3K/Akt/HIF-1α signaling.
  • Vitexin demonstrates potential as a novel therapeutic agent for gastric cancer treatment.
Keywords:
Epithelial-Mesenchymal transitionGastric cancerHypoxiaPhosphatidylinositolsVitexin

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