CANCELLED EMT and back again: does cellular plasticity fuelneoplasticprogressi on?
Epithelial-mesenchymal transition (EMT) is a cellular transdifferentiation program that facilitates organ morphogenesis and tissue remodeling in physiological processes such as embryonic development and wound healing. However, a similar phenotypic conversion is also detected in fibrotic diseases and neoplasia, in which it is associated with disease progression. EMT in cancer epithelial cells often appears to be an incomplete and bi-directional process. Here 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 the Ras-controlled signaling mediators, ERK1, ERK2 and PI3-kinase, as microenvironmental responsive regulators of EMT.
- Research Organization:
- Lawrence Berkeley National Lab. (LBNL), Berkeley, CA (United States)
- Sponsoring Organization:
- USDOE Director. Office of Science. Biological andEnvironmental Research
- DOE Contract Number:
- DE-AC02-05CH11231
- OSTI ID:
- 928784
- Report Number(s):
- LBNL-62604; R&D Project: 443180; BnR: KP1104010; TRN: US200811%%335
- Journal Information:
- Nature Clinical Practice Oncology, Vol. 5; Related Information: Journal Publication Date: 05/01/2008
- Country of Publication:
- United States
- Language:
- English
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