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Background &amp; Objective <p>Weitiao No. 3 decoction (WD-3), a clinically used adjuvant therapy for advanced gastrointestinal tumors, lacks clarified mechanisms in gastric cancer (GC).</p> Methods <p>We profiled chemical constituents by liquid chromatography-mass spectrometry (LC-MS), predicted putative targets and pathways via network pharmacology, evaluated binding by molecular docking, and validated pharmacological effects in MGC-803 cells and mouse xenograft models.</p> Results <p>LC–MS identified 344 constituents; network analyses yielded 188 putative targets and highlighted core nodes (e.g., AKT1, EGFR, PIK3CA, PPARG). Pathway enrichment and docking converged on the PPARγ (PPARG)/AMPK axis. Experimentally, WD-3 suppressed proliferation and migration, induced G1-phase arrest, and increased PPARγ and phospho-AMPK; perturbation of PPARγ modulated AMPK activation and anti-tumor effects. In vivo, high-dose WD-3 reduced xenograft tumor growth in a dose-dependent manner without overt hepato-renal histopathologic toxicity.</p> Conclusions <p>Using LC-MS, network pharmacology, docking, and in vitro/in vivo assays, we found that WD-3 suppresses GC cell proliferation/migration and xenograft growth, accompanied by increased total PPARγ and AMPK Thr172 phosphorylation, supporting involvement of the PPARγ/AMPK axis.</p>

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A Clinically Derived TCM Decoction (WD-3) Attenuates Malignant Phenotypes of Gastric Cancer through the PPARγ–AMPK Pathway

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年1月7日

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  • Hengzhou Zhu,
  • Wenyue Zhao,
  • Jingyi Qian,
  • Xiaodan Zhu,
  • Chencen Zhang,
  • Yuqing Geng,
  • Yun Yuan,
  • Yuetong Xia,
  • Lei Huang,
  • Jiejie Fan,
  • Liang Ma,
  • Valeriy Smirnov,
  • Chunhui Jin

摘要

Background & Objective

Weitiao No. 3 decoction (WD-3), a clinically used adjuvant therapy for advanced gastrointestinal tumors, lacks clarified mechanisms in gastric cancer (GC).

Methods

We profiled chemical constituents by liquid chromatography-mass spectrometry (LC-MS), predicted putative targets and pathways via network pharmacology, evaluated binding by molecular docking, and validated pharmacological effects in MGC-803 cells and mouse xenograft models.

Results

LC–MS identified 344 constituents; network analyses yielded 188 putative targets and highlighted core nodes (e.g., AKT1, EGFR, PIK3CA, PPARG). Pathway enrichment and docking converged on the PPARγ (PPARG)/AMPK axis. Experimentally, WD-3 suppressed proliferation and migration, induced G1-phase arrest, and increased PPARγ and phospho-AMPK; perturbation of PPARγ modulated AMPK activation and anti-tumor effects. In vivo, high-dose WD-3 reduced xenograft tumor growth in a dose-dependent manner without overt hepato-renal histopathologic toxicity.

Conclusions

Using LC-MS, network pharmacology, docking, and in vitro/in vivo assays, we found that WD-3 suppresses GC cell proliferation/migration and xenograft growth, accompanied by increased total PPARγ and AMPK Thr172 phosphorylation, supporting involvement of the PPARγ/AMPK axis.