Role of epithelial-mesenchymal transition in gastric cancer initiation and progression

Abstract

Gastric cancer is one of the most common malignant tumors worldwide. Due to its intricate initiation and progression mechanisms, early detection and effective treatment of gastric cancer are difficult to achieve. The epithelial-mesenchymal transition (EMT) is characterized as a fundamental process that is critical for embryonic development, wound healing and fibrotic disease. Recent evidence has established that aberrant EMT activation in the human stomach is closely associated with gastric carcinogenesis and tumor progression. EMT activation endows gastric epithelial cells with increased characteristics of mesenchymal cells and reduces their epithelial features. Moreover, mesenchymal cells tend to dedifferentiate and acquire stem cell or tumorigenic phenotypes such as invasion, metastasis and apoptosis resistance as well as drug resistance during EMT progression. There are a number of molecules that indicate the stage of EMT (e.g., E-cadherin, an epithelial cell biomarker); therefore, certain transcriptional proteins, especially E-cadherin transcriptional repressors, may participate in the regulation of EMT. In addition, EMT regulation may be associated with certain epigenetic mechanisms. The aforementioned molecules can be used as early diagnostic markers for gastric cancer, and EMT regulation can provide potential targets for gastric cancer therapy. Here, we review the role of these aspects of EMT in gastric cancer initiation and development.