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Role of c-mesenchymal-epithelial transition pathway in gastric cancer

Iacopo Fioroni1, Emanuela Dell'Aquila, Francesco Pantano

  • 1University Campus Bio-Medico Rome - Medical Oncology, via Alvaro del Portillo , 200, 00128, Rome , Italy e.dellaquila@unicampus.it.

Expert Opinion on Pharmacotherapy
|April 18, 2015
PubMed
Abstract

Insights

Gastric cancer remains a significant health challenge. Targeting mesenchymal-epithelial transition (MET) may offer new therapeutic strategies for patients with advanced disease and resistance to other treatments.

Area of Science:

  • Oncology
  • Molecular Biology
  • Drug Development

Background:

  • Gastric cancer is a leading cause of cancer mortality globally, often diagnosed at an incurable stage.
  • Trastuzumab and ramucirumab are approved therapies for specific gastric cancer subsets, highlighting targeted treatment advancements.
  • Research is exploring novel compounds targeting molecules like c-MET to improve patient outcomes and reduce toxicity.

Purpose of the Study:

  • To review the role of c-MET in gastric cancer biology and its potential as a therapeutic target.
  • To discuss the implications of MET activation in gastric cancer progression and treatment resistance.

Main Methods:

  • Investigation of drugs targeting mesenchymal-epithelial transition (MET), mammalian target of rapamycin (mTOR), and polo-like kinase 1 (PLK1).
  • Analysis of MET gene copy numbers in gastric cancer patients (10-20% show increased copy numbers).
  • Evaluation of MET pathway activation's association with aggressive phenotypes and reduced survival.

Main Results:

  • MET activation promotes tumor proliferation, motility, invasiveness, and angiogenesis.
  • Increased MET gene copy numbers are linked to a more aggressive gastric cancer phenotype and poorer survival.
  • The MET/hepatocyte growth factor pathway may contribute to resistance against EGFR/HER2 inhibitors.

Conclusions:

  • The role of c-MET in gastric cancer requires further conclusive evaluation in diverse populations.
  • MET pathway activation serves as a negative prognostic factor in gastric cancer.
  • Targeting c-MET could potentially overcome resistance mechanisms to existing therapies like EGFR/HER2 inhibitors.
Keywords:
c-mesenchymal–epithelial transition inhibitorc-mesenchymal–epithelial transition pathwaygastric cancermolecular targeted agents

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