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A Clinically Derived TCM Decoction (WD-3) Attenuates Malignant Phenotypes of Gastric Cancer through the PPARγ-AMPK
Hengzhou Zhu1, Wenyue Zhao1, Jingyi Qian2
1Department of Oncology, Wuxi Affiliated Hospital of Nanjing University of Chinese Medicine, 8 Zhongnan West Road, Wuxi, Jiangsu, 214071, China.
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.
Insights
Weitiao No. 3 decoction (WD-3) suppresses gastric cancer progression by activating the PPARγ/AMPK pathway. This traditional therapy shows promise for treating gastrointestinal tumors, enhancing cellular mechanisms against cancer growth.
Area of Science:
- Integrative oncology
- Traditional Chinese Medicine pharmacology
- Molecular mechanisms of cancer
Background:
- Weitiao No. 3 decoction (WD-3) is an adjuvant therapy for advanced gastrointestinal tumors.
- Its precise mechanisms in gastric cancer (GC) remain unclear.
Purpose of the Study:
- To elucidate the molecular mechanisms of WD-3 in gastric cancer.
- To investigate the anti-tumor effects and underlying pathways of WD-3.
Main Methods:
- Chemical profiling using liquid chromatography-mass spectrometry (LC-MS).
- Network pharmacology for target and pathway prediction.
- Molecular docking for binding evaluation.
- In vitro (MGC-803 cells) and in vivo (mouse xenograft) validation.
Main Results:
- LC-MS identified 344 constituents; network analysis revealed 188 targets, highlighting AKT1, EGFR, PIK3CA, and PPARG.
- Pathway analysis and docking converged on the peroxisome proliferator-activated receptor gamma (PPARγ)/AMP-activated protein kinase (AMPK) axis.
- WD-3 suppressed GC cell proliferation and migration, induced G1 arrest, and increased PPARγ and phospho-AMPK levels.
- In vivo studies showed dose-dependent reduction in xenograft tumor growth without significant toxicity.
Conclusions:
- WD-3 exerts anti-tumor effects in gastric cancer by modulating the PPARγ/AMPK pathway.
- The findings support WD-3's clinical use and provide mechanistic insights for its adjuvant therapy role.
