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The basics of epithelial-mesenchymal transition
Raghu Kalluri, Robert A. Weinberg
Raghu Kalluri, Robert A. Weinberg
Published June 1, 2009
Citation Information: J Clin Invest. 2009;119(6):1420-1428. https://doi.org/10.1172/JCI39104.
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Review Series

The basics of epithelial-mesenchymal transition

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Abstract

The origins of the mesenchymal cells participating in tissue repair and pathological processes, notably tissue fibrosis, tumor invasiveness, and metastasis, are poorly understood. However, emerging evidence suggests that epithelial-mesenchymal transitions (EMTs) represent one important source of these cells. As we discuss here, processes similar to the EMTs associated with embryo implantation, embryogenesis, and organ development are appropriated and subverted by chronically inflamed tissues and neoplasias. The identification of the signaling pathways that lead to activation of EMT programs during these disease processes is providing new insights into the plasticity of cellular phenotypes and possible therapeutic interventions.

Authors

Raghu Kalluri, Robert A. Weinberg

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Figure 1

EMT.

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EMT.
An EMT involves a functional transition of polarized epithelial cel...
An EMT involves a functional transition of polarized epithelial cells into mobile and ECM component–secreting mesenchymal cells. The epithelial and mesenchymal cell markers commonly used by EMT researchers are listed. Colocalization of these two sets of distinct markers defines an intermediate phenotype of EMT, indicating cells that have passed only partly through an EMT. Detection of cells expressing both sets of markers makes it impossible to identify all mesenchymal cells that originate from the epithelia via EMT, as many mesenchymal cells likely shed all epithelial markers once a transition is completed. For this reason, most studies in mice use irreversible epithelial cell–lineage tagging to address the full range of EMT-induced changes. ZO-1, zona occludens 1; MUC1, mucin 1, cell surface associated; miR200, microRNA 200; SIP1, survival of motor neuron protein interacting protein 1; FOXC2, forkhead box C2.

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ISSN: 0021-9738 (print), 1558-8238 (online)

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