Epithelial-mesenchymal transition (EMT) or mesenchymal-epithelial transition (MET) is important in cancer metastasis, and recent studies have shown that EMT is a heterogeneous and dynamic process with intermediary or partial EMT states. Multiple double-negative feedback loops involving EMT-related transcription factors (EMT-TFs) have been identified to regulate the EMT transition state of the cell. This review summarizes the characteristics, biomarkers, and molecular mechanisms of different EMT transition states, as well as the role of EMT transition state in tumor metastasis, with a focus on gastric cancer.
Epithelial-mesenchymal transition (EMT) or mesenchymal-epithelial transition (MET) plays critical roles in cancer metastasis. Recent studies, especially those based on single-cell sequencing, have revealed that EMT is not a binary process, but a heterogeneous and dynamic disposition with intermediary or partial EMT states. Multiple double-negative feedback loops involved by EMT-related transcription factors (EMT-TFs) have been identified. These feedback loops between EMT drivers and MET drivers finely regulate the EMT transition state of the cell. In this review, the general characteristics, biomarkers and molecular mechanisms of different EMT transition states were summarized. We additionally discussed the direct and indirect roles of EMT transition state in tumour metastasis. More importantly, this article provides direct evidence that the heterogeneity of EMT is closely related to the poor prognosis in gastric cancer. Notably, a seesaw model was proposed to explain how tumour cells regulate themselves to remain in specific EMT transition states, including epithelial state, hybrid/intermediate state and mesenchymal state. Additionally, this article also provides a review of the current status, limitations and future perspectives of EMT signalling in clinical applications.
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