Mechanisms of disease: Epithelial-mesenchymal transition - Does cellular plasticity fuel neoplastic progression?

Eva A. Turley; Mandana Veiseh; Derek C. Radisky; Mina J. Bissell

doi:10.1038/ncponc1089

Mechanisms of disease: Epithelial-mesenchymal transition - Does cellular plasticity fuel neoplastic progression?

Eva A. Turley, Mandana Veiseh, Derek C. Radisky, Mina J. Bissell

Cancer Biology

Research output: Contribution to journal › Review article › peer-review

201 Scopus citations

Abstract

Epithelial-mesenchymal transition (EMT) is a phenotypic conversion that facilitates organ morphogenesis and tissue remodeling in physiological processes, such as embryonic development and wound healing. A similar phenotypic conversion is also detected in fibrotic diseases and neoplasia, and is associated with disease progression. EMT in cancer epithelial cells often seems to be an incomplete and bidirectional process. In this Review, we discuss the phenomenon of EMT as it pertains to tumor development, focusing on exceptions to the commonly held rule that EMT promotes invasion and metastasis. We also highlight the role of RAS-controlled signaling mediators, ERK1, ERK2 and phosphatidylinositol 3-kinase, as microenvironmental responsive regulators of EMT.

Original language	English (US)
Pages (from-to)	280-290
Number of pages	11
Journal	Nature Clinical Practice Oncology
Volume	5
Issue number	5
DOIs	https://doi.org/10.1038/ncponc1089
State	Published - May 2008

ASJC Scopus subject areas

Oncology

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title = "Mechanisms of disease: Epithelial-mesenchymal transition - Does cellular plasticity fuel neoplastic progression?",

abstract = "Epithelial-mesenchymal transition (EMT) is a phenotypic conversion that facilitates organ morphogenesis and tissue remodeling in physiological processes, such as embryonic development and wound healing. A similar phenotypic conversion is also detected in fibrotic diseases and neoplasia, and is associated with disease progression. EMT in cancer epithelial cells often seems to be an incomplete and bidirectional process. In this Review, we discuss the phenomenon of EMT as it pertains to tumor development, focusing on exceptions to the commonly held rule that EMT promotes invasion and metastasis. We also highlight the role of RAS-controlled signaling mediators, ERK1, ERK2 and phosphatidylinositol 3-kinase, as microenvironmental responsive regulators of EMT.",

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AB - Epithelial-mesenchymal transition (EMT) is a phenotypic conversion that facilitates organ morphogenesis and tissue remodeling in physiological processes, such as embryonic development and wound healing. A similar phenotypic conversion is also detected in fibrotic diseases and neoplasia, and is associated with disease progression. EMT in cancer epithelial cells often seems to be an incomplete and bidirectional process. In this Review, we discuss the phenomenon of EMT as it pertains to tumor development, focusing on exceptions to the commonly held rule that EMT promotes invasion and metastasis. We also highlight the role of RAS-controlled signaling mediators, ERK1, ERK2 and phosphatidylinositol 3-kinase, as microenvironmental responsive regulators of EMT.

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Mechanisms of disease: Epithelial-mesenchymal transition - Does cellular plasticity fuel neoplastic progression?

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