Epithelial-mesenchymal plasticity in carcinoma metastasis

Epithelial-mesenchymal plasticity in carcinoma metastasis

2013 | Jeff H. Tsai and Jing Yang
The article reviews the role of epithelial-mesenchymal transition (EMT) in carcinoma metastasis, a multistep process involving local invasion, intravasation, transport, extravasation, and colonization. EMT is a developmental program that allows epithelial cells to lose their polarized structure and gain the ability to migrate and invade, which is crucial for tumor progression. The reverse process, mesenchymal-epithelial transition (MET), is also important in metastasis, allowing tumor cells to re-establish an epithelial phenotype at distant sites. Recent studies have highlighted the dynamic nature of EMT/MET during metastasis, with tumor cells often undergoing both processes multiple times. The molecular pathways involved in EMT, including effector molecules, core regulators, and extracellular cues, are discussed, emphasizing the complex interplay between these components. The article also reviews experimental and clinical evidence of EMT and MET in each step of the metastatic process, including malignant conversion, local invasion, intravasation, systemic transport, extravasation, and colonization. Additionally, it explores the potential of targeting EMT/MET in therapeutic approaches to treat metastatic diseases, considering the challenges and opportunities presented by this dynamic program.The article reviews the role of epithelial-mesenchymal transition (EMT) in carcinoma metastasis, a multistep process involving local invasion, intravasation, transport, extravasation, and colonization. EMT is a developmental program that allows epithelial cells to lose their polarized structure and gain the ability to migrate and invade, which is crucial for tumor progression. The reverse process, mesenchymal-epithelial transition (MET), is also important in metastasis, allowing tumor cells to re-establish an epithelial phenotype at distant sites. Recent studies have highlighted the dynamic nature of EMT/MET during metastasis, with tumor cells often undergoing both processes multiple times. The molecular pathways involved in EMT, including effector molecules, core regulators, and extracellular cues, are discussed, emphasizing the complex interplay between these components. The article also reviews experimental and clinical evidence of EMT and MET in each step of the metastatic process, including malignant conversion, local invasion, intravasation, systemic transport, extravasation, and colonization. Additionally, it explores the potential of targeting EMT/MET in therapeutic approaches to treat metastatic diseases, considering the challenges and opportunities presented by this dynamic program.
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