Journal
NATURE CLINICAL PRACTICE ONCOLOGY
Volume 5, Issue 5, Pages 280-290Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ncponc1089
Keywords
epithelial-mesenchymal transition; extracellular matrix; microenvironment; tumor; ERK1; ERK2
Categories
Funding
- NCI NIH HHS [R01 CA064786-04A1, U54 CA126552-020001, R01 CA064786-13, R01 CA064786, R01 CA064786-05, R01 CA064786-06S1, U54 CA126552-030001, R01 CA064786-07S1, R01 CA064786-11S1, U54 CA126552-02S1, R01 CA064786-10S1, R01 CA064786-12, R01 CA064786-10, R01 CA064786-08S1, U54 CA126552-010001, R01 CA064786-11, R13 CA113258-01, R01 CA064786-09S1, R37 CA064786, U54 CA126552, R01 CA064786-06, R01 CA064786-09, R01 CA064786-07, R01 CA064786-08, U54 CA126552-01, U54 CA126552-040001, R37 CA064786-14, R13 CA113258, R13 CA098946-01, U54 CA126552-04, U54 CA126552-03, U54 CA126552-02] Funding Source: Medline
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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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