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Triptonide inhibits the pathological functions of gastric cancer-associated fibroblasts

Zhenfei Wang1, Daguang Ma1, Changshan Wang2

  • 1Affiliated People's Hospital, Inner Mongolia Medical University, Huhhot, China.

Biomedicine & Pharmacotherapy = Biomedecine & Pharmacotherapie
|October 20, 2017
PubMed

Insights

Triptonide effectively inhibits gastric cancer-associated fibroblasts (GCAFs) by restoring microRNA balance, reducing tumor growth and metastasis. This natural compound shows promise for gastric cancer treatment by targeting the tumor microenvironment.

Area of Science:

  • Oncology
  • Pharmacology
  • Molecular Biology

Background:

  • Conventional chemotherapy faces limitations like accelerated tumor metastasis and induced tumor stem cell phenotypes.
  • Targeting tumor-associated fibroblasts (TAFs) is a promising anti-cancer strategy, but effective drugs are scarce.
  • Gastric cancer-associated fibroblasts (GCAFs) promote gastric cancer progression.

Purpose of the Study:

  • To investigate the potential of triptonide in inhibiting the pathological functions of GCAFs.
  • To explore the mechanism by which triptonide affects GCAFs and gastric cancer progression.

Main Methods:

  • Comparison of GCAFs and normal gastric fibroblasts (GNFs) in promoting gastric cancer cell behaviors.
  • Treatment of GCAFs with triptonide and assessment of its effects on cell functions and microRNA expression.
  • Analysis of microRNA-301a and microRNA-149 expression levels in GCAFs and GNFs.
  • Evaluation of triptonide's impact on the secretion of tissue inhibitor of metalloproteinase 2 (TIMP2) and IL-6.
  • Assessment of triptonide's effect on GCAF-induced epithelial-mesenchymal transition (EMT) in gastric cancer cells.

Main Results:

  • GCAFs exhibited enhanced capacities to promote gastric cancer cell colony formation, migration, and invasion compared to GNFs.
  • Triptonide treatment significantly inhibited these pro-tumorigenic capacities of GCAFs.
  • GCAFs showed higher microRNA-301a and lower microRNA-149 expression than GNFs; triptonide reversed this imbalance.
  • Triptonide treatment normalized microRNA expression, leading to increased TIMP2 and decreased IL-6 production in GCAFs.
  • Triptonide abolished GCAFs' ability to induce EMT in gastric cancer cells.

Conclusions:

  • Triptonide effectively inhibits the malignancy-promoting functions of GCAFs by correcting microRNA expression abnormalities.
  • Triptonide represents a promising therapeutic agent for gastric cancer, targeting the tumor microenvironment.
  • Traditional herbs like those containing triptonide are valuable sources for novel anti-cancer drug development.
Keywords:
Gastric cancer-associated fibroblastsMalignancy-promoting capacityMicroRNAsTriptonide

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